POINT OF VIEWSection Editor: Yoram Rudy, Ph.D.

Slow Pathway Ablation for Atrioventricular Nodal ReentryDIPEN SHAH, M.D., MICHEL HAISSAGUERRE, M.D.,* and FIORENZO GAITA, M.D.†

From the Cardiology Division, Hopital Cantonal de Geneve, Geneva, Switzerland; *Service de Rythmologie, Hopital Haut Leveque,Pessac, France; and †Division of Cardiology, Ospedale Mauriziano, Torino, Italy

The dual pathway theory of AV nodal impulse transmis-sion was formulated about 5 decades ago based on func-tional evidence derived from microelectrode studies. Nev-ertheless, the anatomic correlates of these functionalcharacteristics are still being debated. Along the same lines,although the functional endpoint of slow pathway abla-tion—slow pathway abolition or modi� cation—is well ac-cepted, the means to this end can still be argued.

Since the earliest fortuitous surgical cure of AV nodalreentrant tachycardia (AVNRT), it has been appreciated thatmodifying the functional characteristics of tissue in closeproximity to the compact AV node is necessary to achievethis goal. To improve the selectivity of the delivered abla-tive lesion as well as to simplify the procedure, two broadapproaches have been described. The anatomic approachassumes structural stereotypy correlating with functionallocalization so that most laboratories today target the pos-terior inferior third of Koch’s triangle and the region be-tween the coronary ostium and the tricuspid valve lea� et.On the other hand, proponents of the “potential” approachhave described signature electrograms indicating the subja-cent location of the slow pathway and/or its atrionodalapproach.

However, neither approach is entirely exclusive. Electro-physiologic markers of the His bundle, as well as target siteelectrograms with an appropriate AV ratio, are used toindicate the superior limit of Koch’s triangle and the tricus-pid valve, respectively. Less commonly, intracardiac echo-cardiography has been used to obtain anatomic detail—using the membranous septum as a marker of proximity tothe penetrating bundle of His— combined with visualizationof the septal structures in the region between the coronarysinus ostium and the septal lea� et of the tricuspid valve.Successful slow pathway ablation was exclusively achieved2 to 7 mm posterior to the septal lea� et of the tricuspidvalve in the region of the AV muscular septum.1 Whileallowing visualization of endocardial anatomy with cer-tainty, the available data, albeit in small series, do notdemonstrate either greater ef� cacy or safety with this echo-cardiographically guided approach. An empirical strategy tomaximize the ef� cacy of this anatomic approach has been toperform an extended drag lesion from the coronary sinusostium-tricuspid valve edge to within the proximal coronarysinus. Data on comparative ef� cacy and safety are lacking.

The potential-guided approach is based on localizing anelectrogram signature of critical but ablatable segments ofthe tachycardia circuit.2 Understandably, in view of thecomplex three-dimensional structure of the AV node and itsinterface with working atrial myocardium, the crampedlocalization of the essential elements of the reentrant circuit,and the speci� c electrophysiologic characteristics of thecells involved, this has proved to be less straightforwardthan for other reentrant substrates such as an accessorypathway. Distinguishing activation critical to the arrhythmiaonly (as opposed to for normal AV conduction) has proveddif� cult, if not impossible: reasons include the close juxta-position of the elements involved, the relative lack of spatialmapping resolution and stability during the tachycardia, andthe likelihood that such a distinction may not exist. Thus,slow pathway ablation involves eliminating or modifying acomponent of normal AV conduction and, in principle,should be minimized as much as possible. This is mitigatedby the fact that no long-term deterioration of AV conductionhas been reported and that successful slow pathway ablationafter inadvertent fast pathway ablation or in the presence ofa prolonged PR interval has been achieved without produc-ing AV block.

From a clinical electrophysiologic viewpoint, endocardi-ally recorded signals are dif� cult to analyze. Nonuniformanisotropic activation in the triangle of Koch, multilayeractivation of nodal and transitional cells with slow risingaction potentials, and their electrotonic interactions all com-bine to produce multipotential electrograms. In general,sharp, relatively high-amplitude electrograms indicaterapid, high dV/dt phase 1 action potentials typical of work-ing atrial myocardium, whereas rounded, lower-amplitudepotentials occupying some or all of the AH interval corre-late well with activation of transitional or nodal cells withinor in the vicinity of the posterior nodal extension.3 -5 Incanine hearts, proximal and distal AV bundles have beendescribed instead.6 Characteristically, these potentials ex-hibit rate-related decremental conduction accompanied by areduction in amplitude. A timing closely preceding His-bundle activation during long AH anterograde conductionand disappearance during Wenckebach-like periodic AVconduction strengthen the claim for a nodal origin, whereasan earlier timing within the AH interval, near completedisintegration of the potential at long AH intervals, andpersistence during supra-Hisian interruption of AV conduc-tion (during Wenckebach periodicity) suggest an originfrom the transitional cell interface or the posterior nodalextension. Inversion of the normal sequence (atrial activa-tion followed by slow potential) with a timing preceding theretrograde P wave during VA conduction with a posterior

J Cardiovasc Electrophysiol, Vol. 13, pp. 1054-1055, October 2002.

Address for correspondence: Dipen Shah, M.D., Cardiology Division,Hopital Cantonal de Geneve, 24, Rue Micheli-du-Crest, 1211 Geneva,Switzerland. Fax: 4122-372-7229; E-mail: Dipen.Shah@hcuge.ch

1054 Reprinted with permission fromJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Volume 13, No. 10, October 2002

Copyright ©2002 by Blackwell Futura Publishing, Inc.

septal atrial breakthrough during ventricular pacing or echobeats over the retrograde slow pathway also can be shown,although this is easier to demonstrate for the spiky poten-tials that may represent the insertion of atrial myocardiuminto the slow pathway atrionodal interface.

Our inability to precisely analyze the origin of thesepotentials also is related to resolving activation within themyocardium. The recording � eld of microelectrodes is lim-ited, and these electrodes cannot be placed exactly at the siteof extracellular recording electrodes. Optical mapping using� uorescent dyes has been used recently, but the advantagesof a wider � eld notwithstanding, depth resolution of theoptical signal has not been possible. For extracellular po-tential recordings, it has proven dif� cult to resolve activa-tion signatures of multicomponent slow rising potentials.7

From a practical point of view, extracellular slow path-way potentials are relatively widely recorded, frequentlyover at least half of the triangle of Koch. Thus, an anatomy-based selection of sites recording such potentials within theposterior third of Koch’s triangle is pursued in order toreduce the risk of endangering the AV node. Combining thepresence of slow potentials with multicomponent (sharp)atrial electrograms appears to increase the ef� cacy of theapproach. At high rates, slow potential electrograms aredif� cult to discern and catheter instability is a persistentproblem; therefore, targeting and radiofrequency (RF) de-livery are performed during sinus rhythm. Multiple vari-ables affect the achieved lesion size. The high � ow at thelevel of the tricuspid valve generally means that in temper-ature-controlled RF delivery, the power ceiling is reachedbefore the limiting temperature, and relatively high powerscan be delivered with resulting deep and large lesions. Thismay explain the rapid achievement of therapeutically desir-able, as well as undesirable, modi� cations of AV conduc-tion—not infrequently within a few seconds of beginningRF delivery. The safety factor in avoiding AV block isreduced; therefore, much depends upon reducing cathetermalposition through continuous � uoroscopy, encouragingpatient breath-holding or shallow respiration, waiting forisoproterenol washout before RF delivery, and rhythm mon-itoring for evidence of VA dissociation during junctionalrhythm. A relatively rapid sinus rate may conceal junctionalrhythm and, although heating-induced junctional rhythmshave been shown to originate from nodal structures, it hasnot been shown experimentally that loss of 1:1 VA conduc-tion necessarily precedes alteration of anterograde AV con-duction—in the form of PR prolongation for example. Animportant consideration is that arguably the most sensitivesign of encroachment on normal AV conduction—junc-

tional rhythm—requires RF energy to heat the tissue inorder to elicit it.

To further reduce or eliminate the incidence of inadver-tent AV block, catheter stability, as well as the type ofenergy source, may be important. Cryoablation, which al-lows reversible ice mapping, is associated with superiorcatheter stability because of the formation of an adherenticeball and may be an attractive alternative. The corollary ofgreater selectivity of ablation because of smaller lesion sizemay be a dropoff in acute ef� cacy and/or a higher recur-rence rate, although this remains to be shown.

What about other approaches to the slow pathway? Left-sided ablation has not been systematically investigated,understandably because of access and thromboembolic is-sues, but it is an alternative strategy in case of unsuccessfulright-sided ablation. The need for its occasional use in thiscontext correlates with anatomic data, indicating the rarityof a left-sided only posterior nodal extension.

In the clinical context, progress is measured in terms ofef� cacy and safety. The generally similarly high successrates of slow pathway ablation for AVNRT provide littlefuel for the anatomic versus potential approach argument.Safety pro� les—principally the incidence of AV block—also have not been shown to be any different in the pub-lished data. On the other hand, it remains to be seen whethercryomapping can eliminate the low but uncomfortably un-predictable chance of compromising AV conduction whilepreserving ef� cacy and safety.

References

1. Fisher WG, Pelini MA, Bacon ME: Adjunctive intracardiac echocar-diography to guide slow pathway ablation in human atrioventricularnodal reentrant tachycardia. Circulation 1997;96:3021-3029.

2. Haissaguerre M, Gaita F, Fischer B, Commenges D, Montserrat P,d’Ivernois C, Lemetayer P, Warin JF: Elimination of atrioventricularnodal reentrant tachycardia using discrete slow potentials to guideapplication of radiofrequency energy. Circulation 1992;85:2162-2175.

3. McGuire MA, de Bakker JM, Vermeulen JT, Moorman AF, Loh P,Thibault B, Vermeulen JL, Becker AE, Janse MJ: Atrioventricularjunctional tissue. Discrepancy between histological and electrophysi-ological characteristics. Circulation 1996;94:571-577.

4. Inoue S, Becker AE: Posterior extensions of the human compactatrioventricular node: A neglected anatomic feature of potential clin-ical signi� cance. Circulation 1998;97:188-193.

5. Lin L, Billette J, Medkour D, Reid MC, Tremblay M, Khalife K:Properties and substrate of slow pathway exposed with a compact nodetargeted fast pathway ablation in rabbit atrioventricular node. J Car-diovasc Electrophysiol 2001;12:479-486.

6. Racker DK, Kadish AH: Proximal atrioventricular bundle, atrioven-tricular node, and distal atrioventricular bundle are distinct anatomicstructures with unique histological characteristics and innervation.Circulation 2000;101:1049-1059.

7. Nikolski V, E� mov IR: Fluorescent imaging of a dual pathway atrio-ventricular-nodal conducting system. Circ Res 2001;88:e23-e30.

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