Transverse versus longitudinal electrical propagation within the atrioventricular node during dual pathway conduction: Basis of dual pathway electrophysiology and His electrogram alternans (Zhang's phenomenon)

Background

We have discovered and validated that AV node dual pathway conduction results in a new phenomenon termed His electrogram alternans (HEA), which indicates dual inputs rather than a final common pathway from the AV node into the His bundle. However, the electrophysiological basis for AV node dual pathway conduction and HEA has not been clarified. This study was designed to elucidate the electrophysiological basis for dual pathway conduction and HEA.

Methods

By using HEA as an index of dual pathway electrophysiology, action potentials from multiple locations in the superior and inferior AV nodal domains were obtained to monitor electrical propagation during dual pathway conduction in 8 isolated rabbit hearts.

Results

Fibers inside the AV node were generally aligned along the AV conduction axis. During fast pathway (FP) conduction, electrical excitation in the AV node was propagated in a superior to inferior direction across the major fiber orientation. In contrast, slow pathway (SP) conduction occurred when the superior–inferior propagation failed within the superior nodal domain, permitting electrical propagation to proceed in the inferior nodal domain along the fiber orientation in a posterior to anterior direction. In effect, FP activated first the superior distal node, while SP activated first the inferior distal node. This functional dissociation of superior-fast and inferior-slow domains in distal node produced dual inputs into the His bundle.

Conclusions

Transverse versus longitudinal electrical propagation within the AV node produces functional dissociation in the distal node, resulting in superior-fast and inferior-slow inputs into the His bundle and HEA during dual pathway conduction.     

Decremental Conduction in the Posterior and Anterior AV Nodal Inputs

The role for fiber orientation as a determinant of conduction and block in the posterior (slow pathway, SP) and anterior (fast pathway, FP) AV nodal inputs was examined using multiple extracellular bipolar and intracellular microelectrode recordings in the superfused canine AV junction (N = 14). Results: In both inputs, antegrade longitudinal conduction velocity decremented in association with decreased action potential amplitude and dV/dt _max. A similar decrement was also present in the SP transverse to fiber orientation. SP conduction block occurred preferentially near its insertion into the compact AV node with very slow conduction (0.05 ± 0.01 M/sec) preceding conduction block. Distal antegrade FP conduction block occurred before conduction block occurred at more proximal FP sites. Conduction in the distal FP was maintained at a higher velocity (0.11 ± 0.01 M/sec, p < 0.05 vs. SP) before 2:1 conduction block was observed. Conduction velocity, action potential amplitude, and dV/dt _max were not different at any SP or FP site for paired activation transverse and longitudinal to fiber orientation. Conclusions: The data do not demonstrate a role for fiber orientation determining decremental conduction and block in transitional cell AV nodal inputs. Decremental conduction in both the SP and FP inputs is consistent with a proximal-to-distal gradient in resting membrane potential, action potential amplitude, dV/dt _max, and intracellular excitability in transitional cells during antegrade activation.     

Maturational atrioventricular nodal physiology in the mouse

INTRODUCTION: Dual AV nodal physiology is characterized by discontinuous conduction from the atrium to His bundle during programmed atrial extrastimulus testing (A2V2 conduction curves), AV nodal echo beats, and induction of AV nodal reentry tachycardia (AVNRT). The purpose of this study was to characterize in vivo murine maturational AV nodal conduction properties and determine the frequency of dual AV nodal physiology and inducible AVNRT. METHODS AND RESULTS: A complete transvenous in vivo electrophysiologic study was performed on 30 immature and 19 mature mice. Assessment of AV nodal conduction included (1) surface ECG and intracardiac atrial and ventricular electrograms; (2) decremental atrial pacing to the point of Wenckebach block and 2:1 conduction; and (3) programmed premature atrial extrastimuli to determine AV effective refractory periods (AVERP), construct A2V2 conduction curves, and attempt arrhythmia induction. The mean Wenckebach block interval was 73 +/- 12 msec, 2:1 block pacing cycle length was 61 +/- 11 msec, and mean AVERP100 was 54 +/- 11 msec. The frequency of dual AV nodal physiology increased with chronologic age, with discontinuous A2V2 conduction curves or AV nodal echo beats in 27% of young mice < 8 weeks and 58% in adult mice (P = 0.03). CONCLUSION: These data suggest that mice, similar to humans, have maturation of AV nodal physiology, but they do not have inducible AVNRT. Characterization of murine electrophysiology may be of value in studying genetically modified animals with AV conduction abnormalities. Furthermore, extrapolation to humans may help explain the relative rarity of AVNRT in the younger pediatric population.     

Electrophysiology of the Atrio-AV Nodal Inputs and Exits in the Normal Dog Heart

Ablation of Atrionodal Connections. Introduction : We studied the effects of selective and combined ablation of the fast (FP) and slow pathway (SP) on AV and VA conduction in the normal dog heart using a novel epicardial ablation technique.
Methods and Results : For FP ablation, radiofrequency current (RFC) was applied to a catheter tip that was held epicardially against the base of the right atrial wall. SP ablation was performed epicardially at the crux of the heart. Twenty-three dogs were assigned to two ablation protocols: FP/SP ablation group (n = 17) and SP/FP ablation group (n = 6). In 12 of 17 dogs, FP ablation prolonged the PR interval (97 ± 10 to 149 ± 22 msec. P < 0.005) with no significant change in anterograde Wenckebach cycle length (WBCL), Subsequent SP ablation performed in 8 dogs further prolonged tbe PR interval and the anterograde WBCL (117 ± 22 to 193 ± 27, P < O.(M)5). Complete AV block was seen in I of 8 dogs, whereas complete or high-grade VA block was seen in 6 of 8 dogs. In the SP/FP ablation group, SP ablation significantly increased WBCL with no PR changes. Combined SP/FP ablation in A dogs prolonged the PR interval significantly, but no instance of complete AV block was seen. VA block was found in 50% of these cases. Histologic studies revealed that RFC ablation affected the anterior and posterior atrium adjacent to the undamaged AV node and His bundle.
Conclusion : Using an epicardial approach, combined ablation of tbe FP and SP AV nodal inputs can be achieved with an unexpectedly low incidence of complete A V block, although retrograde VA conduction was significantly compromised.     

Mechanisms underlying the reentrant circuit of atrioventricular nodal reentrant tachycardia in isolated canine atrioventricular nodal preparation using optical mapping

The reentrant pathways underlying different types of atrioventricular (AV) nodal reentrant tachycardia have not yet been elucidated. This study was performed to optically map Koch's triangle and surrounding atrial tissue in an isolated canine AV nodal preparation. Multiple preferential AV nodal input pathways were observed in all preparations (n=22) with continuous (73%, n=16) and discontinuous (27%, n=6) AV nodal function curves (AVNFCs). AV nodal echo beats (EBs) were induced in 54% (12/22) of preparations. The reentrant circuit of the slow/fast EB (36%, n=8) started as a block in fast pathway (FP) and a delay in slow pathway (SP) conduction to the compact AV node, then exited from the AV node to the FP, and rapidly returned to the SP through the atrial tissue located at the base of Koch's triangle. The reentrant circuit of the fast/slow EB (9%, n=2) was in an opposite direction. In the slow/slow EB (9%, n=2), anterograde conduction was over the intermediate pathway (IP) and retrograde conduction was over the SP. Unidirectional conduction block occurred at the junction between the AV node and its input pathways. Conduction over the IP smoothed the transition from the FP to the SP, resulting in a continuous AVNFC. A "jump" in AH interval resulted from shifting of anterograde conduction from the FP to the SP (n=4) or abrupt conduction delay within the AV node through the FP (n=2). These findings indicate that (1) multiple AV nodal anterograde pathways exist in all normal hearts; (2) atrial tissue is involved in reentrant circuits; (3) unidirectional block occurs at the interface between the AV node and its input pathways; and (4) the IP can mask the existence of FP and SP, producing continuous AVNFCs.     

Properties and substrate of slow pathway exposed with a compact node targeted fast pathway ablation in rabbit atrioventricular node

INTRODUCTION: The properties and substrates of slow and fast AV nodal pathway remain unclear. This applies particularly to the slow pathway (SP), which is largely concealed by fast pathway (FP) conduction. We designed a new FP ablation approach that exposes the SP over the entire cycle length range and allows for its independent characterization and ablation. METHODS AND RESULTS: Premature stimulation was performed before and after FP ablation with 5.4 +/- 1.9 lesions (300-microm diameter each; overall lesion size 1.4 +/- 0.5 mm) targeting the junction between perinodal and compact node tissues in seven rabbit heart preparations. The resulting SP recovery curve and control curve had the same maximum nodal conduction time (165 +/- 22 msec vs 164 +/- 24 msec; P = NS) and effective refractory period (101 +/- 10 msec vs 100 +/- 9 msec; P = NS). The two curves covered the same cycle length range. However, the SP curve was shifted up with respect to control one at intermediate and long cycle lengths and thus showed a longer minimum nodal conduction time (81 +/- 15 msec vs 66 +/- 10 msec; P < 0.01) and functional refractory period (180 +/- 11 msec vs 170 +/- 12 msec; P < 0.05). The SP curve was continuous and closely fitted by a single exponential function. Small local lesions (2 +/- 1) applied to the posterior nodal extension resulted in third-degree nodal block in all preparations. CONCLUSION: The posterior nodal extension can sustain effective atrial-His conduction at all cycle lengths and account for both the manifest and concealed portion of SP. Slow and FP conduction primarily arise from the posterior extension and compact node, respectively.     

Extra AV nodal Wenckebach periodicity

Extra AV nodal Wenckebach periodicity was diagnosed in seven patients. The most frequent form of this conduction abnormality was an exit block. The underlying block was localized in the sinoatrial junction and in the atria in two patients; the AV junction and the ventricle were the site of the Wenckebach periodicity in one case each. In extra AV nodal exit block, the actual conduction delay is not seen on the ECG and the diagnosis is based on the progressive shortening of the P-P or R-R intervals followed by a pause which is less than twice the shortest P-P (R-R) interval depending on the level of the block. A Wenckebach periodicity in the bundle branches or within the reentry pathway each occurred in one patient. In these forms of Wenckebach periodicity, the diagnosis is established more readily because the conduction delay can be demonstrated on the surface ECG. The clinical significance of extra AV nodal Wenckebach periodicity is discussed.     

Adenosine's effectiveness in long RP' re-entrant tachycardia: additional evidence of the decremental qualities of the retrograde limb.

Adenosine's ability to terminate atrioventricular (AV) re-entrant supraventricular tachycardia is well documented. Typically, termination occurs as a consequence of transient conduction block in the atrioventricular node, a tissue with decremental qualities. However, the atrioventricular node is not always the site of action when adenosine is used on the re-entrant types of long RP' tachycardias. These tachycardias are, in part, characterized by the decremental qualities of the retrograde limb of the tachycardia circuit, which, in turn, are typically exemplified by retrograde Wenckebach during ventricular (VVI) pacing during intracardiac electrophysiology studies. This case report involves adenosine's ability to block conduction in the retrograde limb of the permanent form of junctional reciprocating tachycardia to provide further evidence as to the AV "nodelike" decremental qualities of this limb.     

从慢径消融发生的交界区心律试探房室结双径的本质

７６例慢－快型房室结折返性心动过速（ＡＶＮＲＴ）患者接受房室结慢径消融术。６５例慢径阻断、９例双径存在但ＡＶＮＲＴ不能诱发、２例快径阻断。慢径阻断后，除快径的前传有效不应期（ＥＲＰ）缩短（２８７．０±７９．０ｍｓｖｓ３４４．０±８７．０ｍｓ，Ｐ＜０．０１）外，房室传导的文氏点、２１阻滞点、室房传导的１１点、快径逆传ＥＲＰ、前传和逆传功能不应期均无明显改变。共放电８４１次，其中无交界区心律的３１７次放电，无一次消融成功。６５例慢径阻断者，交界区心律减少或消失。以上结果提示快径和慢径可能是两条各具电生理特性的传导纤维。     

从射频消融探讨房室结双径路的本质和房室结改良的机制

采用两种方法对142例房室结折返性心动过速(AVNRT)患者进行房室结改良。128例慢—快型AVNRT中,83例单纯慢径改良,33例慢径前传和快径逆传同时改良,3例单纯快径逆传改良,7例快径前传和慢径或快径逆传同时改良,2例失败。1例发生永久性Ⅲ度房室传导阻滞;10例快—慢型和4例慢—慢型AVNRT患者均慢径改良成功。总成功率98.6％。平均随访6±4月,4例(2.8％)复发,均再次消融成功。慢径改良后,快径前传有效不应期、维持1:1快径前传最短的心房刺激周期明显缩短(P<0.05),而逆向快径有效不应期、维持1:1快径逆传最短的心室刺激周期无明显变化(P>O.05)。本研究提示:快径和慢径可能是解剖上不同的纤维。慢径前传和逆传可以是同一条纤维,也可以是不同的纤维;快径亦然。     

Mechanisms of atypical atrioventricular Wenckebach periodicity. A theoretical model derived from the concepts of inhomogeneous excitability and electrotonically mediated conduction

To explain the mechanisms of atypical atrioventricular (AV) Wenckebach periodicity, a model of the AV node was theoretically derived from the concepts of "inhomogeneous excitability" and "electrotonically mediated conduction." The theoretical model of the AV node has the following characteristics: (1) increased vagal tone depresses excitability in the AV node, (2) depressed excitability in the AV node is inhomogeneous in both transverse and longitudinal directions, and (3) electrotonically mediated conduction occurs across inexcitable gaps in the AV node. Many features in atypical AV Wenckebach periodicity are explained by the use of this model. Delayed AV conduction is caused mostly by electrotonically mediated conduction across a much-depressed region in the AV node, and thereafter AV conduction is blocked at the same region, resulting in the occurrence of an AV Wenckebach period with gradual lengthening of PR intervals. Occasionally, longitudinal dissociaton and concealed reentry in the AV node occur in the part below (distal to) the above depressed region, resulting in the occurrence of an AV Wenckebach period with sudden marked lengthening of a PR interval. The sinus impulse following such suddenly delayed AV conduction is usually blocked in the AV node as the result of concealed reentry of the preceding impulse.     

Cx43 and dual-pathway electrophysiology of the atrioventricular node and atrioventricular nodal reentry

Fluorescent imaging has revealed that posterior nodal extensions provide the anatomical substrate for the dual-pathway electrophysiology of the atrioventricular (AV) node during normal conduction and reentry. The reentry can be intranodal, or as well as the posterior nodal extensions, it can involve an endocardial layer of atrial/atrial-nodal (A/AN) cells as part of the AV nodal reentry (AVNR) circuit. Using fluorescent imaging with a voltage-sensitive dye and immunolabeling of Cx43, we mapped the electrical activity and structural substrate in 3 types of AVNR induced by premature atrial stimulation in 8 rabbit hearts. In 6 cases, the AVNR pathway involved (1) a fast pathway (FP), (2) the A/AN layer, and (3) a slow pathway (SP). In 4 cases, reentry took the path (1) SP, (2) A/AN layer, and (3) FP. In 2 cases, reentry was intranodal, propagating between the 2 posterior nodal extensions. Immunolabeling revealed that the FP and SP are formed by Cx43-expressing bundles surrounded by tissue without Cx43. Cx43-expressing posterior nodal extensions are the substrate of AVNR during both intranodal and extranodal reentry.     

Effects of atropine on induction and maintenance of atrioventricular nodal reentrant tachycardia.

The electrophysiologic effects of atropine were studied in 14 patients with dual atrioventricular (AV) nodal pathways and recurrent paroxysmal supraventricular tachycardia (PSVT). During PSVT, all patients used a slow pathway (SP) for antegrade and fast pathway (FP) for retrograde conduction. Atropine enhanced both SP antegrade and FP retrograde conduction, shown by a decrease in paced cycle lengths (atrial and ventricular) producing AV and ventriculoatrial block. Five patients had induction of sustained PSVT before and after atropine. Seven patients failed to induce or sustain PSVT before atropine, because of retrograde FP refractoriness. All seven had induction of sustained PSVT after atropine due to facilitation of FP retrograde conduction. Two patients had only single atrial echoes before atropine, reflecting SP antegrade refractoriness. After atropine, sustained PSVT was inducible in one, and nonsustained in the other, PSVT cycle length could be compared in seven patients before and after atropine and decreased from 383 +/- 25 to 336 +/- 17 (p less than 0.05). Thus, in patients with dual AV nodal pathways, atropine facilitated SP antegrade and FP retrograde conduction, shortened cycle length of PSVT and potentiated ability to sustain PSVT.     

Site of conduction delay and electrophysiologic significance of first-degree atrioventricular block in children with heart disease

Associated electrophysiologic abnormalities and site of delay were studied in 20 patients, aged 1.5 to 16.5 years, with congenital heart disease and first-degree atrioventricular (AV) block (PR interval above the 98th percentile for age and heart rate). Eight of the 20 patients with first-degree AV block were studied after 1 or more cardiovascular operations. Refractory periods of the atrium, AV node, His-Purkinje system and ventricle were determined. As a further test for AV nodal integrity, rapid atrial pacing was performed and the cycle at which Wenckebach periodicity occurred was noted. Four groups were identified. Group I included 4 patients (20%) with intraatrial conduction delay (long PA interval). Three patients had depressed sinus nodal function and 1 had depressed AV nodal function. Group II included 7 patients (35%) with AV nodal delay (long AH interval). One patient had sinus nodal depression and 2 had AV nodal depression (prolonged AV nodal refractory period or Wenckebach at a long paced cycle length). Group III included 3 patients (15%) with His-Purkinje delay (long HV interval). Measured functions were normal in all patients. Group IV included 6 patients (30%) with normal or high normal intracardiac intervals with long PR. One patient had sinus nodal dysfunction, 2 patients had long atrial refractory periods, 1 had AV nodal depression; 2 had long refractory period of the His-Purkinje system, and 1 had long ventricular refractory period. Atrial flutter was induced in 1 patient.(ABSTRACT TRUNCATED AT 250 WORDS)     

Determinants of sustained slow pathway conduction and relation to reentrant tachycardia in patients with dual atrioventricular nodal transmission

In 24 patients with dual atrioventricular (AV) nodal pathways, multiple incremental atrial pacing studies were performed to obtain atrial (A) to His (H) basic driven (A₁ and H₁) and extrastimulus (A₂ and H₂) intervals. Discontinuous A₁-A₂ and H₁-H₂ intervals were analyzed for relations between initial coupling times and subsequent A-H responses, and to examine curves of sequential paced cycle lengths (A-A intervals) versus A-H intervals. Seventeen patients showed sustained slow pathway (SP) conduction with demonstration of discontinuous A-A and A-H curves. Sustained SP conduction occurred at critical atrial paced rates when the first paced beat was blocked in the fast pathway (FP) with conduction via the SP. Eleven of these 17 patients had inducible sustained supraventricular tachycardia (SVT). A-H interval during SVT in these 11 patients was closely related to SP A-H interval during atrial pacing at the paced rate comparable to SVT rate (r = +0.89, p < 0.001). The seven remaining patients showed continuous A-A and A-H curves. In three of these seven patients, sustained SVT was inducible, suggesting ability to sustain SP conduction. All of these three patients had continuous A₁-A₂ and H₁-H₂ curves during sinus rhythm so that the first atrial paced beat could not be blocked in the FP for subsequent SP conduction. In the other four of the remaining seven patients, despite block of the first atrial paced beat in the FP with SP conduction, the second paced beat was blocked in the SP so that all subsequent beats resumed FP conduction. In conclusion, sustalned SP conduction in patients with dual AV nodal pathways requires (1) an initiating beat being blocked in the FP, (2) a critical rate cycle length, and (3) the ability of SP for repetitive conduction at critical rates.     

Conduction properties of the antegrade fast and slow AV nodal pathways associated with AV nodal reentrant tachycardia.

To elucidate differences in conduction properties among the normal atrioventricular (AV) node and the antegrade fast and slow dual AV nodal pathways (DAVNPW), AV nodal conduction curves were analyzed quantitatively in 38 patients. Eighteen patients had antegrade DAVNPW with AV nodal reentrant tachycardia (AVNRT) (dual pathways group) and the remaining 20 had smooth AV nodal conduction curves, without evidence of AV nodal dysfunction (control group). The effective refractory period (ERP) of the antegrade fast pathway was longer than that of the normal AV node (at both basic cycle lengths of 700 and 500 msec, p less than 0.01). Although the atrial premature beats were delayed by a longer ERP in the fast pathway, there was no significant difference in the degree of prolongation of AV nodal conduction time related to shortening of the coupling interval (i.e., ratio of A2H2 increment to A1A2 decrement) between these two pathways. On the other hand, the ERP of the antegrade slow pathway was similar to that of the normal AV node. The degree of prolongation of AV nodal conduction time (relative to the shortening of the coupling interval) was greater in the antegrade slow pathway than in the normal AV node. In conclusion, these findings suggest that in DAVNPW with AVNRT: (1) the antegrade fast pathway is similar to the AV node and its conduction properties are unlikely to be better than those of the normal AV node and (2) the antegrade slow pathway has quantitatively poorer conduction properties than the normal AV node, since it has a greater degree of decremental conduction.     

Evidence for Multiple Atrio-AV Nodal Inputs in the Normal Dog Heart

Multiple Atrio-AVN Inputs in Dog Heart. Introduction : Complete AV block after combined fast pathway (FP) and slow pathway (SP) ablation is uncommon. The purpose of this study was to interrupt activation of these and additional inputs by placing a radiofrequency lesion across the interatrial septum between the FP and SP ablation sites.
Methods and Results : In eight anesthetized open chest dogs, FP ablation induced significant A-H prolongation (δA-H: 51±14 msec; P < 0.001) and a shift of earliest retrograde atrial activation from the anterior septum to the region of the coronary sinus (CS) os. Subsequently, ablation of the interatrial septum across the fossa ovalis was successful in 5 of 8 dogs, changing the sequence of atrial activation (A) so that A at the His-bundle electrogram, which initially preceded A at the CS os (18 ± 4 msec vs 46 ± 7 msec, P < 0.01), now followed CS os A (81 ± 31 msec vs 59 ± 20 msec, P < 0.05). Additional ablation of the SP caused a type II Mobitz AV block or complete AV block in 5 of 8 dogs. The four dogs with complete AV block sbowed a stable, high junctional escape rhytbm at a rate of 64 ± 16 beats/min. Pacing between the ablation lesions and the AV node in one dog showed 1:1 AV conduction and Wenckebach-type AV block indicating preserved AV nodal function. Histology showed necrotic changes in the FP and SP transitional cell zones and in the atrial tissue of the interatrial septum. However, the compact AV node. His bundle, and adjacent atria and transitional cells were undamaged.
Conclusion : There are additional AV nodal inputs in the interatrial septum in addition to the anterior FP and posterior SP inputs. Ablation of all of these may be required, if the aim is production of complete AV block proximal to the AV node with a high Junctional escape rhythm.     

Atypical Wenckebach periodicity simulating Mobitz II AV block.

Eleven patients were studied and a total of 144 Wenckebach cycles in the AV node and 118 Wenckebach cycles in the His-Purkinje system were analysed to determine the incidence of typical and atypical Wenckebach periodicity, with particular emphasis on one variant of atypical Wenckebach that may simulate a Mobitz type II block. This pseudo-Mobitz II pattern was defined as a long Wenckebach cycle in which, at least, the last three beats of the cycle show relatively constant PR intervals (variation of no more than 0.02 s in surface leads and no more than 10 ms in His bundle electrograms) and in which the PR interval immediately following the blocked beat is shorter than the PR interval before the block by 0.04 s or more. Atypical Wenckebach cycles were found to be more common than the typical variety at both the AV node (67%) and His-Purkinje system (69%). The pseudo-Mobitz II pattern was seen in 19 per cent of atypical AV nodal Wenckebach periods and in 17 per cent of atypical His-Purkinje system Wenckebach cycles. The need to discern a ''classical'' Mobitz II block from a pseudo-Mobitz II pattern, especially in the setting of an acute inferior myocardial infarction, is emphasised.     

Delineation of AV Conduction Pathways by Selective Surgical Transection: Effects on Antegrade and Retrograde Transmission

Introduction: The role for transitional cells as determinants of AH and HA conduction was examined in the superfused rabbit AV junction.Methods: Bipolar electrodes and microelectrodes were used to record antegrade A-H and retrograde H-A activation, before and after transection of the transitional cell input to the compact AV node.Results: During pacing from the high right atrium, inferior to the coronary sinus os, beneath the fossa ovalis, or on the anterior limbus, AV Wenckebach block (WB) was mediated by identical transitional cells grouped in close apposition to the compact AV node. Paced WB cycle lengths were shorter from the high right atrium (196 ± 12 msec) and inferior to the coronary sinus os (195 ± 8 msec) versus the fossa ovalis (217 ± 9 msec) or anterior limbus (206 ± 11 msec). With His bundle pacing, retrograde HA WB (211 ± 17 msec) was observed within the N cell region within the compact AV node. After transection of posterior and superior transitional cell input to the compact AV node, the antegrade AH WB cycle length was prolonged (245 ± 18 msec), with an increased WB incidence within the NH region (compact AV node)(5% to 41%; p = 0.014). The incidence of retrograde HA WB determined within the NH region was increased (30% to 88%), with a decrease in the stimulus-fast pathway conduction time (98 ± 7 to 49 ± 6 msec; p < 0.01).Conclusions: The data demonstrate (1) a common transitional cell population determining AH WB, independent of atrial stimulation site, and (2) a plasticity of transitional cell-compact AV node connections, with rapid AH and HA conduction favored by removal of posterior/superior AV nodal input.Supported by a grant from the American Heart Association, Oklahoma Affiliate.