The spontaneous initiation of typical AVNRT is almost always by an APD that is associated with a long P-R and A-H interval leading to a tachycardia in which the atria and ventricles are activated nearly simultaneously (Fig. 8-4). Thus, in typical AVNRT, initiation is produced when an APD blocks in the fast pathway and conduction proceeds antegradely over the slow pathway and retrogradely over the fast pathway, as depicted in Figure 8-1. It is logical to assume that if spontaneous APDs were the most frequent method of initiation of AVNRT, then programmed atrial extrastimuli could simulate the spontaneous situation and induce the tachycardia. In nearly 100% of patients with a history of AVNRT their arrhythmia can be induced by programmed stimulation, most commonly by timed APDs introduced over a reproducible range of coupling intervals (Fig. 8-5).¹⁵,¹⁶,¹⁷,¹⁸,²⁷,⁴³,⁴⁹ In some instances, catecholamines and/or atropine are needed
to facilitate induction. We have actually required stimulation during a 30-degree tilt to induce AVNRT in three patients. The zone of coupling intervals of atrial extrastimuli that induces A-V nodal echoes or sustained SVT (i.e., “echo or tachycardia zone”) usually begins at coupling intervals associated with a marked prolongation of the P-R and A-H intervals. A-V nodal conduction delay (i.e., the increase in A-H interval), and not the coupling interval of the APD, is of prime importance in the genesis of A-V nodal reentrant SVT.⁵⁰ This can be demonstrated by initiation of AVNRT by using the alternative method of atrial pacing to produce A-H delays at longer cycle lengths than at the coupling intervals of single extrastimuli required to produce comparable A-H delays (Fig. 8-6). If one compares the initiation of SVT by atrial extrastimuli with that by atrial pacing, one can demonstrate that only after sufficient A-V nodal conduction delay is achieved, as reflected by the A-H interval, SVT is induced (Fig. 8-7).

Dual pathways are identified by a discontinuous response of A-V nodal conduction time to progressively premature APDs. Dual pathways can be identified by either plotting the A₁-A₂ coupling intervals against the resultant A₂-H₂ intervals or the A₁-A₂ intervals against the H₁-H₂ intervals. A typical dual-pathway curve is depicted in Figure 8-8. At longer coupling intervals, conduction proceeds over the fast (beta) pathway. At a coupling interval of 370 msec, a marked jump in the A-H interval is observed as the impulse blocks in the refractory beta pathway and proceeds slowly along the alpha pathway. Single A-V nodal echoes and SVT appear only during antegrade conduction down the slow pathway and retrograde conduction up the fast pathway. In approximately 25% of the cases, one does not see either an A-V nodal echo or SVT immediately after block in the fast pathway. In a smaller number of cases conduction proceeds down the fast pathway and the slow pathway producing a one-to-two response. An echo or SVT is observed only after a critical A-H interval is reached during slow-pathway conduction that allows the fast pathway to recover excitability and conduct retrogradely (Fig. 8-9). As seen in Figure 8-10, despite block in the fast pathway and very slow conduction down the slow pathway, AVNRT does not occur during high-right atrial stimulation. SVT is induced from the coronary sinus but only after a critical A-H in the slow pathway
is reached. Thus, relating these events to the proposed mechanism shown in Figure 8-1, one must conclude that typical nodal reentry is initiated by atrial stimulation producing block in the fast pathway with a jump to the slowly conducting pathway. Only when conduction is slow enough during slow-pathway conduction to allow recovery of the fast pathway does reentry occur.

By definition, in order to diagnose dual pathways in response to atrial extrastimuli, one must observe an increase of at least 50 msec in the A-H interval with a small (i.e., 10 msec) decrease in the coupling interval of the APD.¹⁵,¹⁶,³⁸,⁴⁹ Although the jump is usually in the order of 70 to 100 msec, marked increases in the A-H of several hundred milliseconds can be observed (Fig. 8-11). As mentioned, dual pathways may also be manifested by different P-R or A-H intervals during sinus rhythm or at identical paced rates (Fig. 8-3). A sudden jump in the A-H during atrial pacing may also be a manifestation of dual A-V pathways. We use a similar beat-to-beat change in the A-H interval of 50 msec during atrial pacing as a marker for dual pathways. Baker et al.⁵¹ suggested that another manifestation of dual A-V nodal pathways is the observation of atrial pacing-induced P-R interval exceeding the paced cycle length. This observation has been made only in patients with either overt dual pathways or AVNRT.

An uncommon manifestation of dual pathways is a double response to an atrial extrastimulus. In such an instance, an atrial extrastimulus can result in conduction down the fast pathway, and if conduction down the slow pathway is sufficiently prolonged, a second response to the ventricle can occur, which may be associated with an atrial echo or sustained AVNRT (Fig. 8-12). Occasionally, patients can exhibit spontaneous 1:2 conduction in sinus rhythm producing a nonreentrant tachycardia during sinus rhythm (Fig. 8-13). This situation requires slow enough conduction down the slow pathway that the HPS has time to recover to produce a second response. If conduction down the slow pathway is not long enough, block in the HPS will occur and the one-to-two response will be concealed (Fig. 8-14). Only a few such patients ever manifest spontaneous AVNRT, an example of which is shown in Figure 8-15. This reflects poor retrograde fast-pathway conduction and/or prolonged retrograde fast-pathway refractoriness, or both. In 11/12 cases I have studied AVNRT could be induced following isoproterenol and/or atropine (see Pharmacologic and Physiologic Maneuvers below).

The site of stimulation can affect the ability to initiate dual pathways and induce AVNRT. Although Ross et al.⁵² demonstrated that the site of stimulation may influence the A-H conduction times over the fast and slow pathways, they showed no significant alteration of refractoriness of these pathways or differences in the ease of induction of dual pathways or AVNRT. However, they noted variability of initiation from either site. Our experience differs slightly. We also have found that the conduction times over the fast and slow pathway may be different during high-right atrial and coronary sinus stimulation. The critical A-V nodal delay (i.e., A-H interval) required to initiate the tachycardia is different depending on the site of stimulation and is almost always shorter from the coronary sinus (Figs. 8-16 and 8-17).⁵³ Whether or not these differences are due to true shortening of A-V nodal conduction time because of differential input into the AVN—as suggested by Batsford et al.⁵⁴ and Aranda et al.⁵⁵—or merely are due to apparent shortening of the A-H interval owing to the alteration of the relationship of the atrial electrogram in the His bundle recording and the true onset of A-V nodal depolarization is unclear. A shorter tachycardia cycle length associated with a shorter A-H at initiation would favor anisotropically based differences in conduction and refractoriness. Both of these mechanisms may play a role in individual patients.

In contrast to others, we have observed that dual A-V nodal pathways and reentry are easier to induce from the high-right atrium than from the coronary sinus, although in rare cases, induction of SVT can be accomplished only from the coronary sinus. The use of multiple drive cycle lengths, multiple extrastimuli, and rapid pacing make induction only by coronary sinus stimulation rare. Despite using these methods, we have observed induction of AVNRT by coronary sinus stimulation when high-right atrial stimulation failed in ∼3% of cases in which we performed both high-right atrial and coronary sinus stimulation (Fig. 8-18). We agree with Ross et al.⁵² that in most cases SVT can be induced with stimulation from both sites,



although different coupling intervals or paced cycle lengths may be required (Figs. 8-16 and 8-17). We have also observed that the refractory periods of the fast and slow pathways can differ depending on the site of stimulation. In approximately one-third of our patients, the refractory period of the fast pathway is shorter during coronary sinus stimulation than during high-right atrial stimulation (Figs. 8-10, 8-16, and 8-17). Moreover, as noted above, the critical A-H necessary to initiate AVNRT is greater during high-right atrial stimulation than for stimulation from the coronary sinus.⁵³ This observation is compatible with the concept that the left atrial extension of the AVN is closer to the fast pathway, thus, stimulation from this site allows earlier recovery. Alternatively, it may just be an expression of a different, functionally determined fast pathway based on the site of stimulation. These site-dependent differences in the ability to initiate AVNRT, as well as differences in the refractory periods of the fast and slow pathways, are likely due to different inputs into the AVN with its nonuniform anisotropic nature. Although in some circumstances this may result from differences in the functional refractory periods (FRPs) of the atrium at the site of stimulation, the nonuniform anisotropic structure of the AVN is a more likely explanation. In any case, because of the variability of induction of AVNRT, it is important to stimulate from both the coronary sinus and the high-right atrium.

If single APDs do not result in block in the fast pathway or, if block does occur, but does not result in sufficient A-V nodal delay, then repeated stimulation at shorter drive cycle lengths, which increase A-V nodal refractoriness and prolong conduction of both the fast and slow A-V nodal pathways (Fig. 8-19), or the use of double extrastimuli (Fig. 8-20) or atrial pacing (Fig. 8-6) frequently produce the block and delay required to initiate SVT. Most patients (approximately 85%) with typical A-V nodal reentrant SVT exhibit dual A-V nodal pathways in response to single high-right atrial extrastimuli.¹⁵,¹⁶,¹⁸,²⁴,²⁷,³⁸ Using multiple drive cycle lengths and extrastimuli from both the high-right atrium and coronary sinus, as well as rapid atrial pacing, isoproterenol and/or atropine, dual pathways may be observed in 95% of patients with AVNRT. This is similar to the experience of Chen et al.⁵⁶ Dual pathways in response to APDs may be observed in as many as 25% of patients without SVT. Despite the jump from fast to slow pathway, with very long A-H intervals, these patients never have an atrial echo; hence, one assumes that the major limitation is retrograde conduction over the fast pathway (Fig. 8-21). The determinants for AVNRT are discussed later in this chapter.

Multiple pathways may be observed in as many as 5% to 10% of patients. These are characterized by multiple jumps of >50 msec with increasingly premature atrial extrastimuli. This is comparable to the data of Tai et al.⁵⁷ Such patients have AVNRTs with longer cycle lengths and longer ERPs and FRPs of the AVN. It is not uncommon for multiple AVNRTs with different cycle lengths and P–QRS relationships to be present. In general, the pathways with the longest conduction times are ablated more posteriorly in the triangle of Koch, leading some investigators to assert that these fibers are located more posteriorly.⁵⁶,⁵⁷ We have found several exceptions to this finding, and believe these findings may be ascribed to anisotropic propagation in a functionally determined circuit.

Failure to demonstrate antegrade dual pathways in a patient with typical A-V nodal reentrant SVT in response to atrial extrastimuli is usually due to one of three factors:

Programmed ventricular premature depolarizations (VPDs) during ventricular pacing or rapid ventricular pacing can also induce typical A-V nodal SVT, but these techniques are less effective than atrial stimulation and often require pharmacologic modulation of autonomic tone; that is, isoproterenol or atropine. In fact, initiation of typical AVNRT by a VPC delivered in NSR is extremely rare because His–Purkinje refractoriness prohibits an early VPC from reaching the AVN (see below). Rarely a late VPC can enter the AVN and produce concealed conduction so that an appropriately timed sinus beat can initiate AVNRT. In our experience, one or more forms of ventricular stimulation can initiate SVT in approximately 40% of patients with typical AVNRT. This is a higher incidence than that found by Sung et al.²⁶ and Wu,²⁴,⁶⁶ who found ventricular stimulation–induced typical AVNRT in only 10% to 30% of patients. In contrast, atypical AVNRT is induced almost as frequently from the ventricle as from the atrium. In almost all of these patients, atrial stimulation can initiate SVT. Very uncommonly rapid ventricular pacing is the only method by which typical AVNRT can be initiated. Ventricular pacing is three times more effective than ventricular extrastimuli in initiating typical AVNRT (Figs. 8-24 and 8-25). If VPDs can initiate typical AVNRT, rapid ventricular pacing also can. In patients with typical AVNRT, retrograde conduction is usually very good and occurs over the (fast) beta pathway. Retrograde block to the atrium over the fast pathway rarely occurs in patients with typical AVNRT initiated by ventricular stimulation (Fig. 8-26), and when it occurs, suggests that the atrium is not required for AVNRT. In either case, ventricular stimulation must produce block in the slow pathway (concealed), conduction up the fast pathway, with subsequent recovery of the slow pathway in time to accept antegrade conduction over it to initiate the ventricular echo, and sustained tachycardia. Rapid ventricular pacing can induce concealed block in the slow pathway and SVT more easily than ventricular extrastimuli. With ventricular extrastimuli, the initial site of delay and/or block is in the His–Purkinje system. Even when conduction proceeds retrogradely over the His–Purkinje system, because of delay in the His–Purkinje system, the S₁-H₂ or V₁-H₂ remains constant. As a result, the prematurity with which the impulse reaches the AVN is fixed (see Chapter 2). Thus, induction of typical AVNRT by a single VPD during ventricular pacing only succeeds in approximately 10% of patients.

Specific reasons for failure to initiate typical AVNRT by VPDs include (a) block in the His–Purkinje system; (b) the
FRP of the His–Purkinje system exceeds the effective refractory period (ERP) of the slow pathway in the retrograde direction; (c) the ERP of the slow pathway is equal to that of the fast pathway in the retrograde direction; (d) the antegrade slow pathway ERP exceeds the ventricular-paced cycle length, therefore it cannot accept an input from the fast pathway at that cycle length; (e) following its engagement from the fast pathway, there is insufficient antegrade delay in the slow pathway to allow the fast pathway to recover; and (f) block in a lower final common pathway in the AVN (i.e., proximal to the slow and fast pathways in the retrograde direction), which thereby prohibits block in one of these pathways. Pacing at shorter drive cycle lengths may increase the percentage of patients in whom typical AVNRT can be induced by ventricular stimulation because of shortening the ERP and FRP of the His–Purkinje system.

Many of the problems imposed by His–Purkinje refractoriness on induction of typical AVNRT by ventricular stimulation can be overcome by rapid ventricular pacing, during which the AVN is the primary site of delay. This explains why rapid pacing is more likely to longitudinally dissociate fast and slow pathways in the AVN than extrastimuli. The observation that ventricular pacing does not always induce typical A-V nodal SVT is explained in part by the occurrence of repetitive concealment, not block, in the slow pathway, rendering it incapable of antegrade conduction. Block cannot be distinguished from concealment in humans.

The specific mechanisms by which ventricular stimulation can induce A-V nodal reentrant SVT follows:

Some generalizations can be made regarding the determinants for developing typical AVNRT. Although dual A-V nodal pathways are required for AVNRT, they are insufficient. Many patients can demonstrate “dual pathways” but do not have spontaneous or inducible AVNRT. The most common finding in patients with dual A-V nodal pathways who do not develop SVT is the failure of the impulse to return up the fast pathway once antegrade conduction has proceeded over the slow pathway. There are four possible explanations for this phenomenon: (a) longitudinal dissociation of the AVN is not really present, but the pattern of conduction of “pseudo-dual” pathways is produced by electrotonic propagation across a nonhomogenous linear area in the AVN, as described previously²⁹; (b) the APD that “blocks” in the fast pathway produces postdepolarization refractoriness (i.e., a manifestation of concealed conduction) resulting in the inability of the fast pathway to recover excitability in time to be reexcited; conduction down the slow pathway is insufficiently slow to allow the fast pathway to recover; (c) the fast pathway has a long retrograde refractory period, which renders it incapable of retrograde conduction despite slow antegrade conduction of the slow pathway; (d) there is no distal connection between the fast and slow pathways. Based on our data and that of others⁶⁷ the most common reason for failure to induce typical AVNRT in patients with antegrade dual pathways is that the fast pathway is incapable of rapid retrograde conduction.

This can be evaluated by using the maximum rates of 1:1 antegrade and retrograde conduction as indices of antegrade slow pathway refractoriness and retrograde fast pathway refractoriness. Denes et al.⁶⁷ first analyzed fast and slow pathway properties in detail and clearly showed that the ability to induce typical AVNRT required 1:1 V-A conduction. Absence of induction of typical AVNRT in patients with antegrade dual pathways was associated with either no V-A conduction or V-A Wenckebach at relatively long drive cycle lengths.⁵⁸ Most often, the ability to induce typical AVNRT requires the capability of one-to-one retrograde V-A conduction at paced ventricular cycle lengths of ≤400 msec.

Although retrograde fast-pathway characteristics determine if reentry can occur, slow-pathway conduction time determines when it will occur. Thus, the “critical A-H” concept depends on fast-pathway recovery at a given A₂-H₂ interval. When echoes do not occur as soon as the impulse blocks in the fast pathway and goes down the slow pathway, concealed conduction into the fast pathway by A₂ may be present, requiring a critical A-H for recovery. This can mimic a primary impairment of V-A fast-pathway conduction as the determinant of reentry. One can recognize the likely presence of concealment if the A-H interval not producing an echo exceeds the shortest cycle length of 1:1 retrograde conduction up the fast pathway.

Although an isolated A-V nodal echo can occur as long as V-A conduction is present, the ability to initiate sustained SVT also requires the capability of the slow pathway to sustain repetitive antegrade conduction. Denes et al.⁶⁷ found that sustained, typical AVNRT was initiated only if the slow pathway maintained 1:1 antegrade conduction at cycle lengths less than 350 msec. Patients who only had single A-V nodal echoes in response to APDs usually developed antegrade Wenckebach in the slow pathway at relatively long cycle lengths. Thus, the ability to initiate sustained SVT depends on the balance of a retrograde fast-pathway conduction and antegrade slow-pathway conduction.

Retrograde fast-pathway conduction appears to be the major determinant of the ability to initiate isolated A-V nodal echoes and/or sustained SVT. This is further supported by the fact that there is no difference in maximal A-H intervals during slow-pathway conduction in patients with and without echoes or SVT. The ability to initiate A-V nodal echoes by APDs thus depends primarily on the capability of V-A conduction over the fast
pathway. This has been our experience almost universally. It is therefore obvious that patients with retrograde dual pathways will have a low incidence of sustained typical AVNRT, because the presence of dual pathways suggests relatively poor retrograde conduction over the fast pathway. Thus, even if 1:1 V-A conduction is present at cycle lengths of less than 400 msec, AVNRT usually occurs only in patients in whom retrograde conduction is maintained over the fast pathway. In an analysis of retrograde dual A-V nodal pathways, Strasberg et al.⁶⁸ found that they could induce typical AVNRT in approximately 20% of patients presenting with retrograde dual A-V nodal pathways. In those cases, retrograde dual pathways (i.e., block in the retrograde fast pathway) occurred at relatively short coupling intervals or short-paced cycle lengths. In our experience, only 5% of patients with retrograde dual A-V nodal pathways will develop typical AVNRT in the baseline state. We have found the use of atropine or isoproterenol, which shortens the retrograde refractory period of the fast pathway and improve retrograde fast-pathway conduction, increases the number of patients with retrograde dual pathways in the control state in whom sustained typical AVNRT can be induced by APDs to 20%. Others have found a slightly higher incidence.⁶⁷,⁶⁸,⁶⁹,⁷⁰ In our patients, facilitation of induction of typical AVNRT depended on improving V-A conduction such that 1:1 V-A conduction over the fast pathway at cycle lengths of 425 msec or less was achieved in all patients in whom typical AVNRT could be induced. Thus, the markers that are predictive of a low likelihood of inducibility of typical AVNRT are (a) no V-A conduction, (b) V-A conduction worse than A-V conduction with retrograde Wenckebach at long cycle lengths (500 msec or more), and (c) retrograde dual pathways. Exceptions can occur if failure of V-A conduction results from retrograde block in the HPS or in a lower final common pathway in the AVN (see subsequent discussion). In the latter case, catecholamines and/or atropine can overcome the block. In addition, as noted earlier in the chapter (and to be discussed later) A-V nodal tachycardia can occur with block to the atrium; retrograde fast pathway is present but not manifested by atrial activation.

The A-H interval may be a useful marker in predicting the capability of rapid V-A conduction. In our experience, as well as that of Bauernfeind et al.,⁷¹ the shorter the A-H interval, the better the V-A conduction. In fact, the shorter the A-H interval, the shorter the antegrade refractory period of the fast pathway, the shorter the cycle length at which block is produced in the fast pathway, and the shorter the cycle length at which 1:1 V-A conduction is maintained. In addition, although overlap existed, Bauernfeind et al.⁷¹ found statistically significant relationships between retrograde H-A intervals and antegrade A-H intervals, shorter cycle lengths maintaining 1:1 V-A conduction and A-H interval, and a higher incidence of inducible SVT in patients with short A-H intervals and dual pathways than in those with longer A-H intervals and dual pathways.⁶⁴ These findings provide a potential explanation for the high incidence of SVT in patients with short P-R intervals giving rise to the so-called Lown–Ganong–Levine syndrome. It is of interest that Akhtar¹⁸ also found that the shortest cycle length of typical A-V nodal SVT correlated best with the shortest cycle length of 1:1 V-A conduction, a finding that correlates with a short A-H interval. In contrast, we have found that the cycle length of SVT is more closely related to conduction down the slow pathway than the A-H interval in sinus rhythm or the H-A during SVT.⁷² Although in patients more than 45 years old the H-A interval and cycle lengths are longer than in patients less than 45, the absolute duration of the A-H is more closely related to the AVNRT cycle length than to the H-A interval.⁷² Spontaneous or pharmacologic-mediated changes in SVT cycle lengths are also more closely associated with changes in slow-pathway conduction. Our findings, which appear to contradict those of Akhtar,¹⁸ grew out of a study examining a different aspect of AVNRT than Akhtar’s study. He was trying to determine the limiting factor for tachycardia rate while we were analyzing factors controlling the tachycardia rate. Spontaneous termination of typical AVNRT can occur by either retrograde block in the fast pathway or antegrade block in the slow pathway. Although it is not always possible to predict which pathway will be the major limiting factor in maintaining AVNRT in an individual patient, a short P-R interval suggests that the fast pathway is unlikely to be the site of block. In addition, the direction (i.e., A-V or V-A) at which conduction fails at the longest cycle length provides a reasonable, but not absolute, marker for induction of spontaneous block.

Little data exist for the determinants of induction of atypical AVNRT because it is such an uncommon arrhythmia. It is our impression that retrograde slow-pathway conduction is the major determinant inducing this arrhythmia. Antegrade fast-pathway conduction is usually rapid enough and refractoriness is short enough to accept and conduct antegradely the impulse that has conducted retrogradely over the slow pathway. Thus, the development of atypical AVNRT by ventricular stimulation is determined primarily by the ability to demonstrate retrograde slow-pathway conduction, since the fast pathway almost always can return the impulse toward the ventricle. When the uncommon form of AVNRT is induced by atrial stimulation, the major determinant of retrograde slow-pathway conduction is insufficient antegrade concealment into the slow pathway so that retrograde conduction is possible.

The sequence of retrograde atrial activation during typical A-V nodal reentrant tachycardia is more complex than previously believed. While early studies suggested that the initial site of retrograde atrial activation during typical AVNRT is recorded in the His bundle electrogram,¹⁶,¹⁸,⁷³,⁷⁴,⁷⁵ more detailed mapping using a decapolar catheter with 2-mm interelectrode distance to record the His bundle (distal pair) and electrograms along the tendon of Todaro, a deflectable quadripolar catheter (2-5-2–mm interelectrode distance) at the base of the triangle of Koch (area between the os of the coronary sinus and tricuspid annulus), and a decapolar catheter (5-mm interelectrode distance) in the coronary sinus with the proximal pair placed 1 to 2 cm inside the os
(Fig. 8-29).⁷⁶,⁷⁷ of the triangle of Koch and coronary sinus shows marked heterogeneity in the pattern of activation.⁷⁶,⁷⁷ Patterns were described along the tendon of Todaro as sequential or broad and throughout the triangle of Koch and coronary sinus as having single or multiple breakthrough sites (Fig. 8-30). Multiple breakthroughs were considered to be present when two or more activation times along the His bundle catheter within 5 msec of each other were separated by two later sites, or when one or more sites on the His bundle catheter and any other catheter (i.e., slow pathway or coronary sinus) occurred within 5 msec of each other. VPDs were introduced when necessary to accurately measure the atrial activation sequence. Examples of heterogenous atrial activation during AVNRT are shown in Figures 8-31 and 8-32 In nearly 50% of patients a secondary breakthrough in the coronary sinus was observed (Fig. 8-29); that is, an electrogram within the coronary sinus was bounded by sites with later electrograms.⁷⁸ Similar findings were observed, but not commented upon by McGuire et al.⁷⁹ Activation during AVNRT and ventricular pacing were discordant qualitatively and/or quantitatively in 60% of patients (Fig. 8-33). Similar heterogeneity was seen during atypical AVNRT although earliest activation tended to be at the base of the triangle of Koch or in the coronary sinus (Fig. 8-34).⁷⁶,⁷⁷,⁷⁸ Multiple breakthroughs, during detailed atrial mapping, are a useful discriminator of AVNRT from atrial tachycardia or circus movement tachycardia using a bypass tract. Although Jackman’s group have described and depicted a number of large reentrant pathways involving the left atrium and coronary sinus, our mapping data have never found and do not support a macroreentrant circuit. The atrial activation pattern during AVNRT has important implications as to the role of the atrium in AVNRT (see discussion below). From these heterogenous activation patterns, the wave of atrial activation subsequently spreads cephalad and laterally to depolarize the remainder of the right and left atria. These findings suggest that retrograde activation during SVT spreads radially after leaving the AVN. Of note, studies by Ross et al.,⁸⁰ using intraoperative mapping, demonstrated a relationship of the earliest site of atrial activation to the retrograde H-A interval. In general, the shorter the H-A interval, the more likely the earliest atrial activation is recorded in the His bundle electrograms. As the H-A interval prolongs, the earliest activation moves closer to the base of the triangle of Koch or in the coronary sinus. Of importance is the recognition that identification of an “earliest” site of atrial activation does not mean that atrial activation is sequential from that site. As stated above, multiple breakthroughs are present in ∼50% of patients. Recent experience using left atrial mapping in addition to detailed right atrial and coronary sinus mapping has confirmed the lack of sequential activation compatible with large reentrant circuits during AVNRT.

On the surface ECG the narrowest P waves are seen when atrial activation begins at the apex of the triangle of Koch. In our experience 7% of AVNRTs have earliest atrial activation
recorded in the coronary sinus, suggesting atrial activation via the left atrial extension of the AVN (Figs. 8-35 and 8-36) All of these patients were successfully ablated from the right side suggesting that the left atrial activation is an epiphenom. Others⁸¹,⁸² have shown a high variability of the earliest site of activation in all varieties of AVNRT which further makes terms like fast-slow; slow-fast, or slow-slow dependent on the anatomic site of retrograde conduction and the R-P relationship, meaningless.

The relationship of atrial activation to the QRS complex is extremely important from a diagnostic standpoint. In approximately 70% of the cases of typical A-V nodal reentrant SVT, the onset of atrial activation (i.e., earliest intracardiac atrial electrogram) appears before or at the onset of the QRS complex. The P wave sometimes begins so early that it gives the appearance of a Q wave in the inferior leads. This is most likely to occur when there is delay between the reentrant circuit and the ventricles. This is most frequent when there is H-V prolongation (Fig. 8-37) but may be observed with delay in the AVN distal to the circuit (Fig. 8-38). In the former case retrograde activation takes place during the H-V interval, and in the latter case retrograde atrial activation begins before the His deflection. This “pseudo-Q wave” is a rare, but relatively specific finding for AVNRT. The presence of atrial activation appearing at or immediately before the onset of the QRS during SVT excludes the possibility of a concealed atrioventricular bypass tract (see following discussion of concealed bypass tracts). The rapid retrograde atrial activation occurs because, as discussed previously, the retrograde limb of the reentrant circuit is the fast beta pathway. In approximately 25% of the tachycardias, atrial activation begins just within the QRS. In 95% of patients, either no discrete P waves are noted on the surface electrocardiogram (40%), or the terminal part of the QRS is slightly distorted, possibly appearing as a “pseudo-S wave” in the inferior leads, a “pseudo-R’” in V₁, or a nonspecific terminal notching (57%). In the remaining patients, the P wave may be seen just after the end of the QRS. Intra-atrial conduction delays can alter the duration of atrial activation so that completion of atrial activation occurs slightly after termination of the QRS. In those patients in whom the P wave distorts the terminal QRS or appears at the end of the QRS, one must distinguish this tachycardia from the circus movement tachycardias using CBTs (see following discussion of concealed bypass tracts). Because completion of atrial activation arising in the midline usually requires at least 50 msec, the appearance of atrial activity as a terminal notch in the QRS, representing the end part of the P wave, suggests that atrial activation begins within the QRS and makes a bypass tract less likely. Sometimes, however, this is hard to distinguish from a bypass tract. In such cases atrial mapping as well as a variety of different responses to ventricular stimulation can help determine whether a bypass tract or atrial tachycardia is present (see following discussion of concealed bypass tracts and atrial tachycardia).

In patients who have the atypical form of AVNRT, the R-P interval is long because retrograde conduction proceeds over the slow pathway. Thus, the R-P/P-R ratio is greater than 1 (long R-P tachycardia). This pattern is extremely uncommon, representing perhaps only 5% of the instances of spontaneous sustained AVNRT in the absence of a prior ablation. The atypical form of AVNRT is often confused with an incessant form of tachycardia caused by a slowly conducting, concealed posteroseptal atrioventricular bypass tract⁶³,⁶⁴,⁶⁵ or an atrial tachycardia arising in the low intra-atrial septum. Atypical AVNRT is more often a paroxysmal arrhythmia, while atrial tachycardias

or those using slowly conducting bypass tracts are frequently incessant and difficult to treat methods to distinguish these arrhythmias are discussed later in this chapter. The R-P intervals discussed above are in the absence of prior catheter ablation. We have noted a greater incidence of atypical R-P relationships and multiple tachycardias in patients postablation.

Bundle branch block is produced by alterations in His–Purkinje conduction and/or refractoriness and therefore should not modify a reentrant process localized to the AVN. If the turnaround site of the reentrant circuit incorporated one of the bundle branches, then bundle branch block or impaired conduction in that proximal bundle branch could alter the tachycardia. The development of prolonged aberration during AVNRT is very uncommon. Of the last 900 consecutively studied patients with A-V nodal reentrant SVT, only 43 developed sustained bundle branch block following induction by APDs; 25 of these had right bundle branch block, and 18 had left bundle branch block. An additional 85 developed ≥5 consecutive complexes manifesting bundle branch block either following induction by ventricular stimulation (19 patients) or, more commonly, following resumption of 1:1 conduction to the ventricles after a period of block below the tachycardia circuit (66/103 patients; see following discussion entitled “Requirement of the Atrium and Ventricle”). All 103 of the patients manifesting block below the tachycardia circuit manifested transient aberrant complexes before normalization of the QRS. In no patient was the AVNRT cycle length (A-A) or H-H interval influenced by the appearance of bundle branch
block. At the onset of bundle branch block, if the H-V interval is prolonged, an increase in the V-V interval equal to the increment in the H-V interval can occur; however, the following V-V time would be shortened by the same amount. During this transition, the A-A and H-H intervals generally remain constant, although if aberration occurs at the onset of the tachycardia, some oscillation of all electrograms can be observed, with some slight slowing prior to resumption of 1:1 conduction. Thus, it is safest to analyze the effects of bundle branch block after induction of the arrhythmia when the tachycardia is stabilized. During the tachycardia, the introduction of VPDs also may occasionally produce transient bundle branch block
(usually left bundle branch block) by retrograde concealment into the bundle branches and/or by rendering the local ventricular myocardium refractory to antegrade depolarization. As in the spontaneously observed appearance of bundle branch block, no change in the A-A or H-H interval results. Whenever the H-V interval prolongs with the development of bundle branch block, the V-V interval also prolongs for one cycle, as mentioned. In this instance, however, because the circuit is not influenced, the A-A interval remains constant and the atrial electrogram, and even the P wave, can be seen before the QRS. The lack of influence of bundle branch block on A-V nodal reentrant SVT is in contrast to patients with SVTs incorporating free-wall bypass tracts (see following discussion). An example of the failure of bundle branch block to influence the tachycardia cycle length is shown in Figure 8-38. In this instance, after a period of left bundle branch block, A-V conduction normalizes. No change in the A-A or V-V intervals occurs during the stable portion of each pattern of ventricular activation.

One of the issues that remains controversial is whether or not the reentrant circuit in AVNRT is entirely subatrial or even intranodal, including “upper and lower” final common pathways, or whether some component of the atrium or His bundle is required (Fig. 8-39). The presence of 1:1 conduction at rapid rates with a short V-A interval, a short H-A interval that remains relatively fixed during SVT, and results of surgical interventions suggest to some that the reentrant circuit involves tissue above and below the AVN.⁸⁰,⁸³ Results of catheter modification of the AVN have also been interpreted similarly (see Chapter 15). Successful ablation of the “fast” pathway at the apex and “slow” pathway at the base of the triangle of Koch has suggested an anatomic construct in which the impulse goes from the fast pathway to the septal atrium, followed by sequential atrial activation to the slow pathway through which the AVN is engaged. Pathologic specimens demonstrating radiofrequency-induced lesions not involving the compact node (no known extent of physiologic influences)
have been used to further support this construct. Still other investigators have taken the relative ease with which AVNRT can be reset from the base of the triangle of Koch as evidence of atrial participation in the circuit.⁴⁶ I believe all of these findings do not prove the requirement of the atrium, but only suggest that the circuit has dimension and/or has different inputs and outputs that are determined by the anisotropic nature of the compact node, its extensions, and the transitional fibers that can be more or less easily engaged depending on the site of stimulation.

I believe that the bulk of the evidence, both experimentally and clinically, suggests that, in most patients, AVNRT is a subatrial reentrant circuit based on the anisotropic properties of the AVN and transitional tissue.⁴¹,⁷⁷,⁷⁸,⁸⁴,⁸⁵,⁸⁶,⁸⁷,⁸⁸,⁸⁹,⁹⁰,⁹¹,⁹² As stated earlier, Efimov et al. using high-density voltage-sensitive dye mapped the AVN three dimensionally and found reentry was subatrial, involving the AVN +/− transitional cells. Cell-to-cell coupling in the AVN is extremely poor due to heterogenous connexins, both type and distribution (primarily connexin 45, with small amounts of connexin 40 near the His bundle) which is the main reason the node is so slowly conducting.

Clinical data, which come from observations during spontaneous SVT, at the time of induction of SVT, and response to stimulation during SVT are discussed in the following paragraphs and are summarized in Table 8-3. They include (a) initiation of AVNRT in the absence of an atrial echo; (b) maintenance of AVNRT in the presence of either a changing V-A relationship, 2:1 retrograde or V-A block and/or A-V dissociation; (c) depolarization of the atrium surrounding the AVN without influencing the tachycardia; (d) resetting AVNRT without atrial activation; (e) heterogenous atrial activation during AVNRT incompatible with atrial participation; and (f) atrial pacing and entrainment of AVNRT with a longer A-H than during the tachycardia entrainment suggesting that little if any of the atrium is required.