Fast Pathway-His Bundle Connections in the Rabbit Heart

Journal of Interventional Cardiac Electrophysiology 10, 121–129, 2004C© 2004 Kluwer Academic Publishers. Manufactured in The Netherlands.

Fast Pathway-His Bundle Connections in the Rabbit HeartEugene Patterson and Benjamin J. ScherlagUniversity of Oklahoma Health Sciences Center, and Departmentof Veterans Affairs Medical Center, Oklahoma City, Oklahoma

Abstract. Objectives: The incidence and the physio-logic roles for direct fast pathway-His bundle connec-tions were examined in 102 rabbit hearts.

Methods: Extracellular bipolar and intracellular mi-croelectrode recordings were made from the super-fused rabbit AV junction.

Results: In 13 of 27 preparations demonstrating an-terior extensions of the fast pathway, the retrogradeHA ERP and 2:1 block cycle length were shortened(128 ± 12 and 145 ± 5 msec, respectively) versus the re-maining 89 preparations (178 ± 15 and 185 ± 10 msec, re-spectively, p< 0.01). The former values were similar tothe ERP and 2:1 block cycle length of fast pathway tran-sitional cells (128 ± 23 and 141 ± 4 msec, respectively),suggestive of a direct fast pathway-His bundle connec-tion. A deflection recorded between the A and H poten-tials of the His bundle electrogram could be dissociatedfrom both atrial and His bundle activation. Intracel-lular microelectrode recordings and light microscopyconfirmed the deflection to be an accessory pathwayconsisting of an anterior extension of fast pathway tran-sitional cells connecting the atrium and His bundle.Transection along the AV groove anterior to the com-pact AV node (N=5) increased the retrograde ERP andWenckebach block cycle length by severing the AH con-nection, or transection of the penetrating bundle (N =4) produced antegrade AH block without altering rapidretrograde conduction.

Conclusions: Fast pathway-His bundle connectionswere present in 13 of 102 rabbit hearts, providing ananatomic and physiologic basis for rapid retrograde VAconduction and a possible retrograde pathway for sus-tained AV nodal reentrant tachycardia.

Key Words. accessory pathways, AV conduction, AVnodal bypass tracts, AV node, AV nodal reentry, retro-grade VA conduction

Introduction

The electrophysiologic properties of retrogradeventriculo-atrial (VA) conduction in individual hu-man hearts demonstrate considerable variation[1–5]. One variant of retrograde conduction is dis-tinguished by abbreviated VA conduction inter-vals (HA <50 msec) and VA refractoriness <AVrefractoriness, with VA conduction intervalsdemonstrating minimal decrement with His bun-dle or ventricular pacing. This variant termedsupernormal retrograde conduction has been

observed in 11 of 100 (11%) [1], in 19 of 124 (15%)[2], in 18 of 104 (17%) [3], and in 6 of 50 (12%)[4] consecutive patients demonstrating both an-tegrade atrioventricular (AV) and retrograde VAconduction. Atrio-Hisian (AH) bypass pathwayshave been postulated to provide the retrograde“pre-excitation” (supernormal retrograde conduc-tion) observed in these patients [1,2].

Supernormal retrograde conduction has alsobeen described in the canine heart with an inci-dence of 2 of 15 (13%) [6] and 4 of 19 (21%) [7].As observed in human hearts, supernormal retro-grade conduction is evidenced as abbreviated VAconduction intervals demonstrating only minimaldecrement with pacing at decreasing cycle lengthsand a retrograde VA block cycle length < the ante-grade AH Wenckebach block cycle length (WBCL).The existence, incidence, and bases for supernor-mal retrograde conduction remain undescribed forthe rabbit AV junction. The present studies wereundertaken to determine (1) the incidence of di-rect atrio-Hisian connections and (2) the relation-ship between direct atrio-Hisian connections andsupernormal retrograde conduction in the super-fused rabbit AV junction.

Methods

Adult New Zealand rabbits of both sexes weigh-ing 2.5–4 kg were anesthetized with intravenoussodium pentobarbital (30 mg/kg). The heart wasremoved and rinsed in Tyrode’s solution (in mM)(NaCl, 130; KCl, 4.05; MgCl2, 1.0; NaHCO3, 20;NaH2PO4, 1.0; glucose, 5.5; and CaCl2, 1.35) bub-bled with 95% oxygen: 5% CO2. The AV junc-tion was pinned in a 20 ml Lucite chamber andsuperfused at 20 ml/min (36◦). Bipolar electro-grams (0.10 mm diameter insulated silver wires,1 mm apart) were obtained (1) inferior to the ten-don of Todaro and superior to the tricuspid an-nulus midway between the coronary sinus os and

Address for correspondence: Eugene Patterson, PhD, 6E103ET CARI, 1200 Everett Drive, Oklahoma City, OK 73104, USA.E-mail: [email protected]

Received 8 August 2003; accepted 23 September 2003

121

122 Patterson and Scherlag

Fig. 1. Rabbit AV junction—A schematic of the rabbit AVjunction is shown including stimulation/recording sites forthe slow pathway (SP) input, fast pathway (FP) input, midpathway (MP) input, and His bundle (HB). Superimposed onthe schematic are microelectrode recording sites from 10 of102 preparations demonstrating two populations of anteriortransitional cells developing 2:1 conduction block out-of-phasewith each other during atrial pacing. In 8 of 10 preparations,transitional cells located along the AV groove (the anteriorextent of the fast pathway) demonstrated prolongedrefractoriness compared to transitional cells located along theanterior limbus.

apex of the triangle of Koch (posterior atrionodalor slow pathway input (SP)), (2) along the ante-rior limbus of the fossa ovalis (anterior atrion-odal or fast pathway input (FP)), (3) 2 mm infe-rior to the fossa ovalis (mid pathway input (MP)),and (4) from the proximal His bundle (HB). Therecording sites are shown in Figure 1. Pacing stim-uli were introduced from the high right atriumand the four bipolar recording sites (2 msec du-ration square wave pulses, 2× diastolic thresholdvoltage). Effective refractory periods (ERPs) weredetermined at a paced cycle length of 400 msec us-ing 2 msec duration stimuli at 2× threshold intro-duced at decreasing 5 msec intervals every 8–12paced beats. Transmural incisions were performedusing a scalpel blade.

Bipolar electrograms were individually ampli-fied and filtered at 1–5000 Hz. Intracellular mi-croelectrode recordings were obtained using 10–25 M� glass microelectrodes filled with 3 M KCland a World Precision Instruments electrometer.Permanent recordings were obtained at a paperspeed of 100 mm/sec using a Gould Windografrecorder. All experiments were approved by theInstitutional Animal Care and Use Committees ofthe University of Oklahoma Health Sciences Cen-ter and the Oklahoma City Department of Veter-ans Affairs Medical Center.

StatisticsData are expressed as the mean ± the standard er-ror of the mean. Differences between groups weredetermined by analysis of variance for paired orunpaired data as appropriate followed by Scheffe’stest. Criterion for significance was p ≤ 0.05.

Results

Conduction Along the Anterior Limbus ofthe Fossa Ovalis—The Anterior FastPathway InputDuring pacing at cycle lengths greater than theAH WBCL, 1:1 activation was maintained in tran-sitional cells located along the anterior limbusof the fossa ovalis (anterior AV nodal input, orfast pathway input). Transitional cells of the ante-rior input could be differentiated from atrial my-ocardium by the observation of 2:1 block (neverWenckebach block) at heart rates maintaining1:1 activation of atrial myocardium (Fig. 2). Con-duction along the anterior limbus was decremen-tal. The site of 2:1 block moved proximally alongthe anterior limbus as the paced atrial rate wasincreased (Fig. 2). 2:1 Block within transitionalcells of the anterior input however determined 2:1AH conduction block at rapid atrial heart rates(Fig. 2).

Fast Pathway ExtensionsExtracellular bipolar electrograms and microelec-trode recordings demonstrated two distinct pop-ulations of superficial anterior transitional cellsin 27 of 102 rabbit AV junction preparations. Onepopulation extended along the anterior limbus ofthe fossa ovalis to the tricuspid valve, overlyingthe compact AV node (normal anterior AV nodalinput). The second population projected anteriorto the compact AV node and central fibrous body,roughly parallel to the AV groove. In 10 prepara-tions, different refractory periods were observedin these two transitional cell populations (Figs. 1and 3). Both transitional cell populations demon-strated only 2:1 block, and never demonstratedWenckebach block. 2:1 Conduction block was ob-served at paced cycle lengths maintaining 1:1atrial activation. The refractoriness of transitionalcells in the anterior extension was prolonged com-pared to transitional cells extending over the com-pact AV node in 8 of 10 AV junctional preparations(Fig. 2). The differential refractoriness was notsolely the result of decremental conduction sincethe pattern of 2:1 block was discordant within thetwo cell populations (Fig. 3).

Supernormal Retrograde HA ConductionSupernormal retrograde conduction was observedin 13 of 102 consecutive experiments (Table 1).Supernormal retrograde VA conduction was de-fined as (1) 2:1 HA block at paced cycle lengths<170 msec and (2) retrograde H-FP intervals≤50 msec, with an HA decrement ≤10 msec dur-ing His pacing at decreasing cycle lengths from1000 msec until 2:1 HA block was observed. In all13 preparations, microelectrode recordings were

AV Nodal Bypass Pathways 123

Fig. 2. Rate-dependent decrement in the fast pathway AV nodal input—microelectrode recordings were made from transitionalcells at two sites located along the anterior limbus of the fossa ovalis, a site near the fossa ovalis (FP1) and a site near the compactAV node (FP2). Bipolar electrograms were recorded from the proximal fast pathway (halfway between the inferior fossa ovalis andthe tricuspid valve annulus), and from the His bundle (HB). Note that during AV Wenckebach block (175 msec), 1:1 conduction ismaintained in both atrial myocardium and transitional cells of the anterior fast pathway input. At shorter paced cycle lengths, 2:1AH conduction block is initially observed reflecting 2:1 block within superficial transitional cells along the anterior limbusdownstream to the distal ME recording site (FP2) near the compact AV node. The site of 2:1 block moves more proximally along theanterior limbus (to FP1) with further decreases in the paced cycle length. 2:1 Block in transitional cells of the anterior inputdetermines 2:1 AH conduction. 1:1 Conduction is maintained within atrial myocardium to a paced cycle length of 100 msec (notshown).

obtained from tissue comprising a direct connec-tion from the atrium to the His bundle, anteriorto the compact AV node. Examples are shown inFigures 4 and 5. In 8 of the 13 preparations,a distinct electrogram previously described byAlanis8 was observed during the AH interval ofthe His bundle electrogram (Fig. 5). Activationof the Alanis potential coincided with the mi-croelectrode recording from the bypass pathway.Both the microelectrode recording and the Alanispotential could be dissociated from AH conductionthrough the AV node and from atrial activationduring pacing from the high right atrium. AH WBblock was observed at atrial cycle lengths of 180–225 msec with 1:1 atrium-bypass tract activationmaintained to 125–143 msec cycle lengths, disso-ciating bypass tract activation from antegrade AVconduction and His bundle activation. 1:1 Atrial,but not bypass tract activation potential activa-tion remained at atrial cycle lengths <120 msec.1:1 Retrograde HA activation was maintained toa 130–160 msec cycle length. A retrograde by-pass pathway is further implicated by the short,

32 msec HA interval observed during His bundlepacing compared with a 130–142 msec AH inter-val. Summary data (Table 2) confirm the exam-ples shown in Figure 4 (intracellular microelec-trode recording) and Figure 5 (Alanis potential).

In each of the 8 rabbit AV junctions demonstrat-ing an Alanis potential, intracellular microelec-trode recordings confirmed a transitional tissuepathway projecting anterior to the central fibrousbody and activated concordantly with the Alanispotential. Reduced resting potential, reduced ac-tion potential amplitude, and prolonged action po-tential duration (compared to atrial myocardium),consistent with superficial transitional fibers ofthe anterior input were recorded (Figs. 4 and 5,Table 3). Local 2:1 block of bypass pathway ac-tivation was observed at cycle lengths exceedingatrial refractoriness (Table 3). Retrograde con-duction over the bypass pathway was determinedby His bundle refractoriness in each preparation(Figs. 4 and 5).

Refractoriness of the normal AV conductionsystem exceeded refractoriness of the bypass


Fig. 3. Recordings from the anterior limbus (FP2) and anterior to the central fibrous body (FP1)—Microelectrode recordings wererecorded from superior right atrial endocardium (A), anterior limbus halfway between the lower edge of the fossa ovalis and thetricuspid valve annulus (FP2), and along the AV groove anterior to the central fibrous body (FP1). A bipolar electrogram recordingboth fast pathway and His bundle activation was recorded immediately superior to the central fibrous body (FP (eg)). With highright atrial pacing at 150 bpm, 1:1 local and AH activation is observed. At 285 bpm, 2:1 alternans is observed in the anterior fastpathway extension (FP1) and 2:1 block is observed in the FP electrogram. At 360 bpm, 2:1 block is observed in the anterior fastpathway extension (FP1) and alternans is present in the normal fast pathway (FP2). At 380 bpm (157 msec cycle length), 2:1 block,out-of-phase at FP1 versus FP2, is present. 1:1 atrial activation is maintained.

pathway in each experiment (Fig. 4 and Table 3).In Figure 4 (upper panel), AH conduction blockis observed at a 200 msec atrial cycle lengthwith bypass pathway activation maintained to a143 msec cycle length. With His bundle pacing(lower panel), 1:1 retrograde HA conduction wasmaintained to a 130 msec cycle length with ret-rograde 2:1 conduction block determined by Hisbundle refractoriness.

In 5 of 13 preparations demonstrating super-normal retrograde conduction and an AV bypasspathway, antegrade pre-excitation of the His bun-dle could be demonstrated at prolonged atrial cyclelengths >500 msec (AH interval = 62 ± 13 msec)with a sudden shift to a more prolonged AH inter-val (110±18 msec) with high right atrial pacing at

Table 1. AH and HA conduction in the Rabbit AV junction

SP-Pacing MP–Pacing FP-Pacing HB-Pacing Antegrade AH interval Retrograde HAAH WBCL AH WBCL AH WBCL HA WBCL or (High right atrial interval (HB(msec) (msec) (msec) 2:1 block (msec) pacing) (msec) pacing) (msec)

Normal (N = 89) 181 ± 12 200 ± 10† 188 ± 10 218 ± 10‡ 94 ± 6 116 ± 11Supernormal retrograde 172 ± 7 191 ± 7 173 ± 5 145 ± 5∗ 102 ± 12 39 ± 12∗

conduction (N = 13)

∗ p < 0.01 vs. Normal.† p < 0.03 vs. SP-Pacing and FP-Pacing.‡ p < 0.02 vs. SP-Pacing, MP-Pacing, and FP-Pacing.WBCL: Wenckebach block cycle length, SP: slow pathway input, MP: mid pathway input, FP: fast pathway input, HB: His bundle.

367 ± 18 msec (p < 0.05). Antegrade 2:1 AH con-duction block was observed between the bypasstract and the His bundle with a shorter refractoryperiod existing for 2:1 conduction block betweenthe atrial and the bypass tract (Table 2).

Surgical Transection of the AV BypassSurgical transection was performed along the AVgroove parallel to the His bundle in 5 prepara-tions, severing the bypass pathway. Severing thebypass pathway did not alter the antegrade AHWBCL or AH interval (Table 4) while prolong-ing HA intervals and retrograde HA block cyclelengths (Table 4). Retrograde HA conduction blockwas transformed from 2:1 block to Wenckebachblock (N = 5) (Fig. 6).


Fig. 4. Microelectrode recordings from a fast pathway-His bundle bypass pathway—In the upper panel, an intracellularmicroelectrode recording (BYPASS TRACT) from a proposed fast pathway-His bundle bypass pathway is shown during atrialpacing. Bipolar electrode recordings are shown from the fast pathway input (FP (eg)), and the His bundle (HB (eg)). An Alanispotential is present in the FP electrogram (marked by ∗). With incremental pacing, AH conduction fails at an atrial cycle length of220 msec and 1:1 activation of the fast pathway-His bundle bypass pathway is maintained to a atrial cycle length of 170 msec. Inthe lower panel, retrograde HA conduction is shown during His bundle pacing. 1:1 retrograde His-fast pathway conduction ismaintained to a cycle length of 170 msec.

Isolation of the AV Bypass Connection byTransection of the Proximal His BundleThe penetrating portion of the His bundle wastransected in 4 experiments. Antegrade conduc-tion over the bypass pathway was observed in only2 of 4 preparations with retrograde conductionmaintained in all 4 preparations (Table 5). An ex-ample is shown in Figure 5. Pre-transection, theAH WBCL was 175–185 msec. 1:1 Activation ofan Alanis potential was maintained to a 160 mseccycle length. 1:1 Retrograde HA activation wasmaintained to a 135 msec cycle length. Follow-ing surgical transection of the penetrating bun-dle, antegrade AH activation was maintained to a330 msec cycle length, with antegrade AV blockoccurring between the bypass pathway and theHis bundle. Retrograde conduction over the by-

Table 2. Incidence of AV nodal bypass pathways in the Rabbit AV junction

Antegrade AH Antegrade alanis HA 2:1 block over Retrogradeconduction using potential 2:1 retrograde bypass alanis potential

(N = 102) bypass pathway (msec) block (msec) pathway (msec) (msec)

Incidence N = 5 (5%) N = 8 (7%) N = 13 (13%) N = 8 (7%)ERP (msec) 267 ± 39 146 ± 8 150 ± 12 150 ± 82◦ block (msec) 261 ± 33 142 ± 9 145 ± 4 146 ± 6

ERP: effective refractory period.

pass pathway was maintained to a cycle length<150 msec with 2:1 block determined within theHis bundle.

Light MicroscopyThree formalin-fixed, paraffin-embedded AV junc-tion preparations demonstrating rapid retrogradeVA conduction were sectioned (8 µ) at right an-gles to the AV bundle axis. Every 5th section wasstained with hematoxylin-eosin or trichrome. Di-rect AH connections were observed in two of thethree preparations (Fig. 7). The connections con-sisted of narrow, elongated atrial fibers resemblingtransitional cells projecting through the centralfibrous body (N = 1), or passing anterior to thecentral fibrous body to insert adjacent to the Hisbundle/left bundle (N = 1).


Fig. 5. Transection through the central fibrous body—(upper panel)—A microelectrode recording from the His bundle and bipolarelectrograms (mid pathway input (MP), fast pathway input (FP), and His bundle (HB) are shown during slow pathway pacing andduring His bundle pacing prior to transection of the penetrating bundle within the central fibrous body. With incremental slowpathway pacing, 2:1 AH conduction block is present at a cycle length of 175–185 msec. 1:1 activation of the Alanis potential ismaintained to a 160 msec cycle length. With incremental His bundle pacing, 1:1 stimulus—fast pathway activation is maintainedto a 135 msec cycle length when 2:1 block is observed. (Lower panel)—Microelectrode recordings were obtained from site A (anintracellular potential corresponding with the Alanis potential in the HB electrogram) and site B (HB). With incremental pacingfrom the slow pathway input after penetrating bundle transection, AH conduction is maintained to a 330 msec cycle length.Paroxysmal AH block is observed despite continued activation of the accessory pathway. With His bundle pacing, 1:1 Hisbundle-fast pathway activation is maintained to a cycle length of 150 msec demonstrating asymmetry of AH and HA activation overthe bypass pathway.

Discussion

Supernormal retrograde conduction is observedin a minority of human [1–6], canine [6,7], andrabbit hearts. The incidence of supernormal ret-rograde conduction in man ranges from 2 of

18 (11%) [1] to 18 of 104 (17%) [3] consecutivepatients demonstrating both AV antegrade andretrograde VA conduction. In another study eval-uating 13 patients with supraventricular tachy-cardia, but without clinical evidence for ante-grade pre-excitation (short PR interval), five of 13


Table 3. Asymmetric conduction in the fast pathway—Hisbundle pathway

Antegrade Retrograde(N = 8) conduction conduction Atrium

RMP (mV) −72 ± 4 −72 ± 3 −79 ± 2∗APA (mV) 76 ± 6 78 ± 7 98 ± 6∗APD50 (msec) 106 ± 9 108 ± 5 73 ± 9∗APD90 (msec) 132 ± 8 133 ± 12 116 ± 8∗Local 2:1 block (msec) 135 ± 8† 132 ± 9 <100Antegrade WBCL (msec) 286 ± 13 – –HA 2:1 BLOCK (msec) – 132 ± 11† –

∗ p < 0.03 vs. FP—HB bypass pathway.† p < 0.001 vs. Antegrade WBCL.RMP: resting membrane potential, APA: action potential amplitude,APD90: action potential amplitude at 90% of repolarization, ERP: ef-fective refractory period, WBCL: Wenckebach block cycle length overbypass pathway.

patients demonstrated rapid retrograde conduc-tion. The VA interval was short, with little decre-ment during ventricular pacing, and without pro-longation of the VA activation interval followingverapamil administration [4]. Gomes et al. [5] sim-ilarly described short VA intervals with little rate-dependent decrement in 7 of 12 patients with slow-fast AV nodal reentrant tachycardias.

Bypass pathways consisting of (1) an insulatedintranodal tract [1], (2) “atrial” fibers bypassingthe AV node [1,2], (3) an atrio-nodal tract bypass-ing the AV node [1], or (4) atrial fibers enter-ing the lower endocardial surface of the AV nodeclose to the AV node [1] have been hypothesizedto provide for the short retrograde HA conductiontimes and reduced retrograde VA refractorinesscharacterizing supernormal retrograde conduc-tion. Histologic data are limited. Brechenmacher[9] described an autopsy series of 687 hearts frompatients with heart disease, most having ventric-ular conduction disturbances. From a single block,8 µ thick sections were made in the frontal planethrough the interatrial and interventricular sep-tum. Only two cases demonstrated an atrio-Hisbundle tract. One patient died from supraven-tricular tachycardia with a rapid ventricular re-sponse and the other patient died suddenly inassociation with aortic stenosis. In both the for-mer case [10] and the latter case [9], musculartracts descended from the interatrial septum tothe lower part of the atrioventricular bundle. Morerecently, Gollob et al. [11] described a single an-terior accessory AV node producing ventricularpre-excitation and comprising the retrograde limbof an AV reentrant tachycardia. The low histo-logic incidence of atrio-His bundle bypass path-ways contrasts with a much higher incidence ofelectrophysiologic connections in man [1–5], dog[6,7], and rabbit (present studies). In the rabbit,intracellular recordings were made from transi-

Fig. 6. Transection of the AV accessory pathway—Upperpanel—A microelectrode recording from the His bundle (HB)is shown during spontaneous atrial rate, atrial pacing (160and 150 msec cycle length), and during His bundle pacing.Bipolar electrograms from the mid pathway input (MP), fastpathway input (FP), and His bundle are also shown. 1:1 AVconduction is present during a spontaneous atrial rhythm at400 msec. Retrograde HA block is observed at a 170 msec cyclelength, and is observed with minimal decrement precedingblock. Lower panel—Bipolar and intracellular microelectroderecordings are shown post-transection along the AV groove.Antegrade conduction is maintained at a paced cycle length of320 msec. With His bundle pacing, the stimulus—A interval isprolonged (100 msec) compare to pre transection (22 msec).Wenckebach HA block rather than 2:1 block is present, at acycle length of 210 msec versus 170 msec pre AV cut.

tional tissue extending anterior to the central fi-brous body and connecting with the His bundle.This electrical connection could be (1) maintainedfollowing transection of the penetrating AV bun-dle and (2) severed by transection along the AVgroove.


Table 4. Transection of a FP—HB bypass pathway

Antegrade AH 2:1 Retrograde AH interval HA interval(N = 5) WBCL (msec) HA block (msec) (msec) (msec)

Pre-Transection 186 ± 12 136 ± 12 112 ± 16 48 ± 8Post-Transection 188 ± 11 201 ± 18∗ 114 ± 18 116 ± 9†

∗ p = 0.01; † p = 0.001.FP: fast pathway input, WBCL: Wenckebach block cycle length.

Table 5. Transection of the penetrating bundle

Antegrade AH 2:1 Retrograde AH interval HA interval(N = 4) WBCL (msec) HA block (msec) (msec) (msec)

Pre-Transection 188 ± 16 142 ± 12 112 ± 16 38 ± 8Post-Transection 360 (N = 2)∗ 146 ± 16 60 (N = 2)† 36 ± 9

∗ p = 0.02; † p = 0.04.WBCL: Wenckebach block cycle length.

The data from the present studies are con-sistent with an atrio-Hisian pathway providedby transitional cells [12,13]. Pathway activationcould be separated from both atrial and His bun-

Fig. 7. Light microscopy—Four sagittal sections of the AV junction (trichrome staining) are shown anterior to the fibrous collar,from anterior to posterior over an approximate 2.5 mm distance. Atrial transitional fibers can be seen to enter the His bundle at thesite where the left bundle exits (left hand picture). Only the distal end of the AH connection can be seen in this histologic section. Theatrial insertion was observed in histologic sections obtained 2.5 mm more posterior to the present tissue section (right hand section).A thinning of the central fibrous body containing narrow transitional cells can be observed in the present histologic section (markedby white arrows in the two center panels). The pathway taken by the transitional fiber AH connection is through the central fibrousbody.

dle activation with atrial pacing. The resting mem-brane potential, action potential amplitude, actionpotential plateau, effective refractory period, and2:1 block pattern are consistent with descriptions


of superficial transitional cell pathways extend-ing along the anterior limbus of the fossa ovalis,comprising an anterior AV nodal input [12,13].Furthermore, we have described with both histo-logic and electrophysiologic evidence, anterior ex-tensions of transitional cells failing to connect tothe His bundle and thereby failing to provide func-tional bypass pathways.

Asymmetry of AV and VA Activation in theFast Pathway-His Bundle Bypass PathwayLocal antegrade block within the bypass pathway(between atrial and the bypass pathway) is ob-served at shorter cycle lengths than antegrade AHblock through the compact AV node. Despite localbypass pathway activation following transectionof the penetrating bundle, the pathway may failto support AV conduction. Antegrade AH conduc-tion block was present between the bypass path-way and the His bundle. There are, however, nodifferences in the local antegrade 2:1 block cy-cle length in the bypass pathway and the retro-grade 2:1 block cycle length determined in eitherthe His bundle or the bypass pathway. Failureof antegrade AH activation over the pathway isconsistent with insufficient source current from anarrow bypass pathway to provide activation ofa larger His bundle (impedance mismatch) [14].Conversely, the increased ability to conduct in theretrograde direction may also result from a largecurrent source (His bundle) conducting into a nar-row bypass pathway that slowly expands beforefast pathway insertion, with a smaller impedancemismatch at the fiber input.

Clinical SignificanceThe present studies suggest that fast pathway-His bundle pathways may provide for rapid retro-grade activation in man. Such a finding may rep-resent both a physiologic variant and a substratesupporting supraventricular arrhythmia [3,5]. Ina clinical report by Moleiro et al. [15], recurrentsupraventricular arrhythmia and rapid AV con-duction were proposed to occur via an atrio-Hisianbypass tract. In one patient, an Alanis potentialis evident within the AH interval of the His bun-dle electrogram. Future studies will be needed toestablish the role, if any, for retrograde bypasspathways in patients with AV nodal reentranttachycardia.

Acknowledgments

The research was supported by a grant-in-aidfrom the American Heart Association/OklahomaAffiliate, Oklahoma City, Oklahoma, and research

funds from the Department of Veterans Affairs,Washington, DC.

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Fast Pathway-His Bundle Connections in the Rabbit Heart