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Atypical bypass tracts
A working definition of an atypical bypass tract (BT) is a conduction pathway that bypasses all or part of the normal conduction system but is not a rapidly conducting pathway connecting atrium and ventricle near the mitral or tricuspid annulus. Thus, pathways that connect the atrium to the His bundle (HB, atrio-Hisian BT), the atrioventricular node (AVN) to the His-Purkinje system (HPS; nodofascicular BT) or the ventricle (nodoventricular BT), or the HPS to the ventricle (fasciculoventricular BT) fit into this designation ( Fig. 23.1 ). Additionally, a unique type of concealed atrioventricular (AV) BTs exhibits slow and decremental retrograde conduction properties and mediates a rare form of nearly incessant orthodromic AV reentrant tachycardia (AVRT), known as permanent junctional reciprocating tachycardia (PJRT), and will be discussed in this chapter.
Types of Bypass Tracts (BTs).
Right atrium and ventricle are depicted. 1, Atriofascicular BT; 2, long atrioventricular BT; 3, nodofascicular BT; 4, nodoventricular BT; 5, fasciculoventricular BT; 6, atrio-Hisian BT; 7, typical short atrioventricular BT.
“Mahaim fibers”
In 1937, during pathological examination of the heart, Mahaim and Benatt identified islands of conducting tissue extending from the HB into the ventricular myocardium. These fibers were called “Mahaim fibers” or “fasciculoventricular fibers.” This description was subsequently expanded to include connections between the AVN and the ventricular myocardium (nodoventricular fibers). Later, it was recognized that BTs could arise from the AVN and insert into the right bundle branch (RB) (nodofascicular fibers). This classification for Mahaim fibers persisted until evidence suggested that the anatomical substrate of tachycardias with characteristics previously attributed to nodoventricular and nodofascicular fibers is actually atrioventricular (AV) and atriofascicular BTs with decremental conduction properties (i.e., conduction slows at faster heart rates). Although these BTs are sometimes collectively referred to as “Mahaim fibers,” the use of this term is discouraged; it is more illuminating to name the precise BT according to its connections. In this chapter, these BTs are collectively referred to as “ atypical BTs” to differentiate them from the more common ( typical ) rapidly conducting AV BTs that insert into ventricular myocardium near the AV annulus and result in the Wolff-Parkinson-White (WPW) syndrome or concealed BTs. ,
“Mahaim tachycardia”
The term “ Mahaim tachycardia ” is used to describe the typical constellation of electrophysiological (EP) features that characterize the unusual form of reentrant tachycardia using an atypical BT, without implication about the underlying anatomical cause. It should be noted that because the term was originally applied to an anatomical finding and subsequently (incorrectly) applied to physiology that matched what would be expected from this anatomy, it has given rise to more confusion than understanding. Hence, the use of the term Mahaim tachycardia should generally be discouraged; instead, one should simply describe the physiological characteristics of the tachyarrhythmia.
Atypical atrioventricular and atriofascicular bypass tracts
Long decrementally conducting atrioventricular and atriofascicular bypass tracts
Atriofascicular and long AV BTs comprise the majority (80%) of atypical BTs. These BTs predominantly arise from the right atrial (RA) free wall; cross the tricuspid annulus in the lateral, anterolateral, or anterior region; extend along the right ventricular (RV) free wall to the region where the moderator band usually inserts at the apical third of the RV free wall; and insert into the distal part of the RB (atriofascicular BTs) or into the ventricular myocardium close to the RB (long decrementally conducting AV BTs). These BTs are functionally similar to the normal AV junction, with an AVN-like structure leading to an HB-like structure. In essence, these BTs function as an auxiliary conduction system parallel to the normal conduction system (AVN–HPS). Similar to the normal AVN, these BTs demonstrate decremental conduction (related to the slow rate of recovery of excitability) and Wenckebach-type block in response to rapid atrial pacing and are sensitive to adenosine. The conduction delay in these BTs has been localized to the intra-atrial portion of the BT (the AVN-like portion), whereas the interval from the inscription of the BT potential at the tricuspid annulus and the onset of ventricular activation (BT-V interval) remains constant. These BTs are typically unidirectional, conducting only in the anterograde direction; retrograde conduction block in the BT occurs near the atrial insertion.
Short decrementally conducting atrioventricular bypass tracts
These BTs are analogous to the decrementally conducting concealed BTs responsible for permanent junctional reciprocating tachycardia (PJRT) in that they bridge the AV rings and insert proximally into ventricular myocardium in close proximity to the AV annulus. These BTs primarily arise from the RA free wall but can also arise from the posterior or septal region. Left-sided BTs with decremental conduction characteristics have rarely been described. These BTs demonstrate prolonged conduction time over their length (>30 milliseconds) and decremental conduction and Wenckebach-type block in response to rapid atrial pacing. However, they do not consistently appear to be responsive to adenosine. Anterograde conduction block can be observed in approximately two-thirds of patients, suggesting that atypical short AV BTs comprise a heterogeneous group in regard to their nodal-like behavioral features. Similar to atriofascicular BTs, short AV BTs only conduct anterogradely.
An acquired form of short AV decrementally conducting BTs has been reported to be caused by incomplete RF ablation of typical, rapidly conducting AV BTs. These BTs are capable of being part of an arrhythmia circuit. The decrease in conduction velocity may potentially be related to a decrease in cell-to-cell coupling caused by ablation-mediated injury.
Arrhythmias associated with atypical atrioventricular and atriofascicular bypass tracts
Atypical AV and atriofascicular BTs in patients with clinical arrhythmias have the following characteristics: (1) unidirectional (anterograde-only) conduction (with rare exceptions); (2) long conduction times; and (3) decremental conduction.
Atypical BTs comprise 3% to 5% of all BTs. The incidence is slightly higher (6%) in patients presenting with supraventricular tachycardia (SVT) with left bundle branch block (LBBB) morphology. Multiple BTs occur in 10% of patients with atypical BTs. In some cases, ventricular preexcitation over a rapidly conducting AV BT can mask the presence of an atypical BT, which only becomes apparent after ablation of the typical BT. Dual AVN pathways or multiple BTs occur in 40% of patients with atypical BTs. Atypical BTs can also be associated with Ebstein anomaly.
Supraventricular tachycardias requiring a bypass tract for initiation and maintenance
Antidromic AVRT can utilize the atypical AV and atriofascicular BT anterogradely and the HPS-AVN retrogradely. Preexcited AVRT can also use the atypical BT anterogradely and a second AV BT retrogradely. In the latter case, the AVN can participate as an innocent bystander mediating anterograde or retrograde fusion.
Because these atypical BTs almost always conduct anterogradely only, they cannot mediate orthodromic AVRT, but they can mediate antidromic AVRT or can be an innocent bystander during other SVTs (e.g., AVN reentrant tachycardia [AVNRT]). However, they can coexist with typical rapidly conducting AV BTs. Right free wall atriofascicular BTs capable of both anterograde and retrograde conduction that participate in both antidromic and orthodromic AVRT have rarely been reported.
Supraventricular tachycardias not requiring a bypass tract for initiation and maintenance
AVNRT, atrial tachycardia (AT), atrial flutter (AFL), or atrial fibrillation (AF) can coexist with atypical BTs, in which case the atypical AV and atriofascicular BTs function as bystanders, wholly or partly responsible for ventricular activation during the tachycardia. Of note, the overall incidence of AF in patients with atypical BTs is low (<2%) and is much lower than in those with the classic WPW syndrome. AVNRT is observed in less than 10% of patients with atypical BT–related tachycardia.
Electrocardiographic features
Normal sinus rhythm
During normal sinus rhythm (NSR), the ECG shows a normal QRS or minimal preexcitation in most patients with atypical AV and atriofascicular BTs. Minimal preexcitation over a right-sided AV BT can be suspected by the absence of the normal septal forces (small q waves) in leads I, aVL, V 5 , and V 6 and the presence of an rS complex in lead III in the setting of a narrow QRS. The presence of an rS complex in lead III in conjunction with the absence of q waves in lead I (caused by depolarization of a discrete portion of the anteroapical region of the RV) appears to be a specific finding for atypical right-sided BTs and can be observed in approximately half of the patients. Also, slurring or notching of the terminal portion of the QRS complex (defined as elevation of the QRS–ST junction, observed mainly in leads I, V 5 , and V 6 ) can be seen in a significant percentage (30%–45%) of patients with decrementally conducting atypical BTs, and this finding can be a clue to the presence of atypical AV and atriofascicular BTs.
The degree of preexcitation depends on the relative conduction time over the AVN and BT. Maneuvers that prolong conduction over the AVN (e.g., atrial pacing, vagal maneuvers, or drugs) to a greater degree than prolongation of BT conduction will increase the degree of preexcitation.
Because atypical AV and atriofascicular BTs exhibit decremental conduction, increasing the atrial pacing rate results in prolongation of the P-delta interval. This is in contrast to the setting with typical rapidly conducting AV BTs, during which progressively faster atrial pacing rates result in increasing delay in AVN conduction, increasing degree of ventricular preexcitation, and a P-delta interval that remains constant regardless of the degree of preexcitation because conduction over the typical BT displays less, or no, decrement compared to the AVN.
Preexcited QRS morphology
For atriofascicular BTs, the preexcited QRS is relatively narrow (133 ± 10 milliseconds) and exhibits a classic LBBB pattern with a frontal axis between 0 and –75 degrees and a late precordial R/S transition zone (at lead V 4 or V 5 , and sometimes V 6 ). A monophasic R wave in lead I and rS pattern in lead V 1 are typically observed. The delta wave, classically seen with BTs inserting into the myocardium near the annuli, is characteristically absent. In contrast, for long decrementally conducting AV BTs (inserting into ventricular myocardium at some distance from the AV annulus, in contrast to atriofascicular tracts that insert into RB), the QRS is relatively wider (166 ± 26 milliseconds) and the LBBB pattern is less typical (with broad initial R in lead V 1 ). The QRS is even wider and the LBBB pattern is less typical with decrementally conducting short AV BTs than that with atriofascicular or long decrementally conducting AV BTs.
Supraventricular tachycardias
Arrhythmias associated with atypical BTs exhibit LBBB morphology and, most often, in the setting of long decrementally conducting AV and atriofascicular BTs, left axis deviation on the surface ECG ( Fig. 23.2 ). Several ECG features suggest (although are not diagnostic of) atriofascicular BTs as the cause of an SVT with LBBB pattern, including (1) QRS axis between 0 and –75 degrees, (2) QRS duration of 150 milliseconds or less, (3) R wave in lead I, (4) rS complex in lead V 1 , and (5) precordial R wave transition in lead V 4 or later.
Electrophysiological testing
Baseline observations during sinus rhythm
In the baseline state, minimal or no preexcitation is present; thus, the His-ventricular (HV) interval is normal or slightly short.
Programmed atrial stimulation during sinus rhythm
Progressively shorter atrial pacing cycle lengths (PCLs) or atrial extrastimulus (AES) coupling intervals produce decremental conduction in both the atypical BT and, to a greater degree, the AVN ( Fig. 23.3 ). Consequently, the atrio-His (AH) interval increases, the QRS morphology gradually shifts to a more preexcited LBBB morphology, and the AV (A-delta) interval increases. However, the AV (A-delta) interval increases to a lesser degree than the AH interval. This is in contrast to the setting of typical rapidly conducting AV BTs whereby the AV (A-delta) interval remains constant despite prolongation of the AH interval and exaggeration of the degree of preexcitation, because the A-delta interval represents the constant, nondecremental conduction time over the typical AV BT.
With progressively shorter atrial PCLs or AES coupling intervals, the HV interval decreases as the His potential becomes progressively inscribed into the preexcited QRS (usually within the first 5–25 milliseconds after the onset of the QRS). The His potential eventually becomes activated retrogradely as the wavefront travels anterogradely down the BT and then retrogradely up the RB to the HB ( Fig. 23.3 ). When the His potential is lost within the QRS, it is unclear whether anterograde AV conduction continues to propagate over the HB or block has occurred.
At the point of maximal preexcitation, the AV (A-delta) interval continues to prolong with more rapid pacing because of the decremental conduction properties of the BT, but the His–QRS relationship remains unaltered because the HB is being activated retrogradely. The fixed VH interval, despite shorter PCLs or AES coupling intervals, suggests that the BT inserts into or near the distal RB at the anterior free wall of the RV with retrograde conduction to the HB. Whenever the VH interval is less than 20 milliseconds, insertion into the RB (i.e., atriofascicular BT) is likely. On the other hand, with long decrementally conducting AV BTs, which insert into the ventricular myocardium close to the RB, the VH interval approximates the HV interval minus the duration of the His potential (because the His potential is activated retrogradely).
For short decrementally conducting BTs, the HB is activated anterogradely, and retrograde conduction to the HB is only seen following AV block or during antidromic AVRT. Decremental conduction (progressive prolongation of the AV interval) and Wenckebach-type block can develop in the BT. The conduction delay in these BTs is localized to the intra-atrial portion of the BT; the interval from the inscription of the BT potential at the tricuspid annulus to the onset of ventricular activation (BT-V interval) remains constant.
Dual AVN physiology is common in patients with atypical BTs. Sometimes, during AES, a jump from the fast to the slow AVN pathway prolongs the AH interval to a degree sufficient to unmask preexcitation over the BT, at which time the His potential becomes inscribed within the QRS.
The site of the earliest ventricular activation during preexcitation is at the RV apex for long, decrementally conducting AV BTs and atriofascicular BTs, but adjacent to the annulus near the base of the RV for short, decrementally conducting AV BTs ( Fig. 23.4 ).
Preexcitation becomes more prominent when atrial stimulation is performed closer to the atrial insertion site of AV or atriofascicular BTs. This is in contrast to the setting of nodofascicular and nodoventricular BTs, whereby the site of atrial stimulation does not influence the degree of preexcitation.
Programmed ventricular stimulation during sinus rhythm
Because these BTs rarely have retrograde conduction, ventriculoatrial (VA) conduction during ventricular pacing is mediated solely by the HPS-AVN with a concentric atrial activation sequence and decremental properties in response to progressively shorter ventricular PCLs or ventricular extrastimulus (VES) coupling intervals. If rapid and fixed VA conduction is present, the presence of a separate retrogradely and rapidly conducting AV BT should be excluded.
Response to physiological and pharmacological maneuvers
Adenosine produces conduction delay or block in most atypical BTs, except for short decrementally conducting AV BTs ( eFigs. 23.1 and 23.2 ). The conduction delay is localized to the intra-atrial portion of the BT (i.e., between atrial and BT electrograms); the interval from the inscription of the BT potential at the tricuspid annulus and the onset of ventricular activation remains constant (analogous to adenosine effects of the AH and HV intervals of the normal AVN-HPS). When adenosine administration slows AVN conduction to a great degree than that in the BT, an increase in the degree of preexcitation is noted in all types of BTs.
Induction of tachycardia
Initiation by programmed atrial stimulation
Initiation of antidromic AVRT by an AES requires the following: (1) intact anterograde conduction over the BT; (2) anterograde block in the AVN or HPS; and (3) intact retrograde conduction over the HPS-AVN once the AVN resumes excitability following partial anterograde penetration. Whereas the latter is usually the limiting factor for the initiation of antidromic AVRT using typical, rapidly conducting AV BTs, it is readily available in the setting of atypical BTs. This is because of the slow decremental conduction anterogradely over the atypical BT, providing adequate delay for full recovery of the HPS-AVN.
As noted, progressively shorter atrial PCLs or (especially from the RA) result in progressive AV (A-delta) interval prolongation and a greater degree of preexcitation until it is maximal. Often, once maximal preexcitation has been achieved, cessation of pacing is followed by preexcited SVT. Progressively shorter AES coupling intervals similarly result in progressive AV (A-delta) interval prolongation and a greater degree of preexcitation until maximal; when anterograde AVN conduction fails but conduction persists over the BT, the HPS-AVN can be activated retrogradely to initiate antidromic AVRT.
The sudden appearance of preexcitation associated with a “jump” from the fast to the slow AVN pathway with a His potential inscribed before ventricular activation or with a VH interval of less than 10 milliseconds strongly favors AVNRT. Although a slowly conducting atriofascicular BT that becomes manifest with a jump to the slow AVN pathway cannot be excluded, a consistent pattern of dual pathway dependence and an HV relationship too short to be retrograde from the distal RB would be unlikely. Induction of AVNRT with AES is almost always associated with a dual pathway response, which may not be seen if the impulse conducts anterogradely over the BT and captures the HB before it is activated by the impulse traversing the slow AVN pathway anterogradely. In other cases, a jump can be seen so that the anterograde His potential follows the QRS with a typical AVN echo to initiate SVT, analogous to 1:2 conduction initiating antidromic AVRT.
Initiation by programmed ventricular stimulation
Initiation of antidromic AVRT by ventricular pacing or VES requires the following: (1) retrograde block in the BT, which is almost always available, because the atypical BTs are usually unidirectional (anterograde only); (2) retrograde conduction over the HPS-AVN; and (3) adequate VA delay to allow for recovery of the atrium and BT so that it can support subsequent anterograde conduction.
Ventricular pacing can initiate SVT in 85% of cases. Initiation is almost always associated with retrograde conduction up a relatively fast AVN pathway, followed by anterograde conduction down a slow pathway, which is associated with preexcitation. The anterograde slow pathway can be a BT (i.e., antidromic AVRT) or a slow AVN pathway (i.e., AVNRT with an innocent bystander BT).
During induction of the SVT by ventricular pacing at a PCL similar to the tachycardia CL (TCL) or by a VES that advances the His potential by a coupling interval similar to the H-H interval during the SVT, comparing the His-atrial (HA) interval following the ventricular stimulus with that during the SVT can help distinguish antidromic AVRT from preexcited AVNRT. The HB and atrium are activated in parallel during AVNRT but in sequence during ventricular stimulation and during antidromic AVRT. Therefore, an HA interval that is longer with ventricular pacing or VES initiating the SVT than that during the SVT suggests AVNRT. This occurs despite the fact that the H 1 -H 2 interval of the VES (i.e., the interval between the His potential activated anterogradely by the last sinus beat to the His potential activated retrogradely by the VES initiating the SVT) exceeds the H-H interval during the SVT. Because the AVN usually exhibits greater decremental conduction with repetitive engagement of impulses than in response to a single impulse at a similar coupling interval, the more prolonged the HA with the initiating ventricular stimulus, the more likely the SVT is AVNRT. In the setting of antidromic AVRT, the BT mediates anterograde conduction; therefore, the HA interval during ventricular pacing or the VES initiating the SVT, at a comparable coupling interval as the TCL, should have the same HA interval as during the SVT.
Tachycardia features
Site of earliest ventricular activation
In the setting of atriofascicular, nodofascicular, and long decrementally conducting AV BTs, the earliest ventricular activation occurs at or near the RV apex. In contrast, for nodoventricular and short decrementally conducting AV BTs, the earliest ventricular activation occurs adjacent to the tricuspid annulus.
Ventricular-His interval
For atriofascicular and nodofascicular BTs, the VH interval is short (16 ± 5 milliseconds), much shorter than the nonpreexcited HV interval and also shorter than the VH interval during ventricular pacing, because the BT inserts into the RB; hence, the HB and ventricle are activated in parallel during antidromic AVRT but in sequence during ventricular pacing. Conduction time to the distal RB is short (V-RB = 3 ± 5 milliseconds). For long decrementally conducting AV BTs, the VH interval is relatively short (37 ± 9 milliseconds) but longer than that of atriofascicular BTs, because the ventricle and HB are activated in sequence, not in parallel. In this setting, the VH interval approximates the HV interval minus the duration of the His potential, because the BT inserts close to the RB and the His potential is activated retrogradely.
In the presence of long decrementally conducting AV BTs, conduction time to the distal RB (V-RB = 25 ± 6 milliseconds) is longer than that for atriofascicular BTs. During antidromic AVRT using a nodoventricular or a short decrementally conducting AV BT, intermediate VH intervals are observed, whereby the His potential is inscribed within the QRS. The VH interval during the AVRT is longer than the nonpreexcited HV interval as well as the VH interval during RV apical pacing, exceeding it by the time it takes the impulse to travel from the ventricular insertion site of the BT at the RV base to the distal RB (i.e., because of the long V-RB interval). When antidromic AVRT occurs in the presence of retrograde right bundle branch block (RBBB), the VH interval is long (the His potential is inscribed after the QRS and the VH interval is longer than the nonpreexcited HV interval). Retrograde block over the RB results in anterograde conduction over the distal RB (in the setting of atriofascicular BTs) or RV and transseptal impulse propagation with subsequent retrograde conduction over the left bundle into the HB and AVN. This results in an antidromic AVRT with a macroreentrant circuit incorporating the left bundle retrogradely and either an atriofascicular, a long decrementally conducting, or a short decrementally conducting AV BT anterogradely.
Atrial-ventricular relationship
For atriofascicular BTs, long decrementally conducting AV BTs, and short decrementally conducting AV BTs, a 1:1 A-V relationship is a prerequisite for the maintenance of antidromic AVRT, because parts of both the RA and the RV are critical components of the reentrant circuit. The AV interval is often more than 150 milliseconds due to the slow conduction properties of the BT. However, in the setting of nodofascicular and nodoventricular BTs, the atrium is neither part of nor required for the reentry circuit, and VA block or AV dissociation can (although rarely) be present without disrupting the SVT.
QRS-VHis interval
The interval between the onset of the QRS to the onset of the ventricular electrogram recorded on the HB catheter measured (QRS-VHis interval) during antidromic AVRT or full preexcitation can help distinguish between the different types of atypical BTs. QRS-VHis intervals shorter than 33 milliseconds favor atriofascicular BTs and long decrementally conducting AV BTs over short decrementally conducting AV BTs. This is expected given that the earliest site of activation is at the AV junction in the setting of short decrementally conducting AV BTs, as compared to the region of the RV incorporating the moderator band in the setting of atriofascicular or long AV BTs.
Response to drugs
These SVTs are very responsive to and terminate easily with adenosine, calcium channel blockers, and beta-blockers.
Changes in tachycardia cycle length
Changes in the cycle length (CL) of antidromic AVRT using an atriofascicular or a long AV BT as the anterograde limb of the circuit can occur secondary to changes in the VA conduction time, due to either retrograde RBBB or shift of retrograde conduction from a fast to a slow AVN pathway. Prolongation of the TCL reflects prolongation of the VH interval in the former setting but prolongation of the HA interval in the latter setting. Additionally, VA conduction over the HB-AVN axis changing into VA conduction over a second BT can alter the TCL. When this occurs, the change in the TCL will depend on the location of the ventricular insertion site of the second BT and the conduction properties of that BT. Therefore, there can be a shortening or a prolongation of the TCL. The behavior of the V-RB and VH intervals in that situation will depend on where the block is located in the RB-HB-AVN axis.
Response to right bundle branch block
The development of RBBB (e.g., secondary to catheter-induced mechanical trauma or VES) during antidromic AVRT increases the size of the reentrant circuit, because the impulse cannot reach the HB through the RB, and it has to travel transseptally and then retrogradely over the left bundle. This results in prolongation in the VA interval and delay in the timing of the next atrial activation and, as a result, prolongation of the TCL. The increment in the VA interval occurs because of prolongation of the VH interval, while the HA interval remains constant.
Diagnostic maneuvers during tachycardia
Programmed atrial stimulation during tachycardia
Resetting.
To prove the presence of a BT and its participation in the SVT, a late-coupled AES is delivered from the lateral RA (close to the BT) when the AV junctional portion of the atrium is refractory (as indicated by the lack of advancement of local atrial activation in the HB or coronary sinus ostium [CS os] recording) so that the AES does not penetrate the AVN. This maneuver is analogous to the introduction of VES when the HB is refractory during orthodromic AVRT. If this AES resets (advances or delays) the timing of the next ventricular activation, it indicates that an anterogradely conducting AV or atriofascicular BT is present and excludes nodoventricular and nodofascicular BTs. If the AES advances (or delays) the timing of the next ventricular activation and the advanced (or delayed) QRS morphology is identical to that during the SVT, this proves that the AV or atriofascicular BT also mediates preexcitation during the SVT, either as an integral part of the SVT circuit or as an innocent bystander (i.e., preexcited AVNRT). On the other hand, if the AES advances the timing of both the next ventricular activation and subsequent atrial activation, it proves that the SVT is an antidromic AVRT using an AV or atriofascicular BT anterogradely and excludes preexcited AVNRT ( Fig. 23.5 ). Advancement of both ventricular and atrial activation by such an AES requires anterograde conduction over the BT followed by retrograde conduction over the AVN. This can occur during antidromic AVRT but not in AVNRT, because in the setting of AVNRT, the HB would be refractory because of anterograde activation by the time the advanced ventricular impulse invades the HPS retrogradely, with subsequent failure of the advanced ventricular activation to penetrate the HPS-AVN and affect the timing of subsequent atrial activation. A short-coupled AES can block in the BT, terminating the SVT (in the setting of antidromic AVRT) or changing the SVT to a narrow QRS complex SVT at the same CL and same HA interval (in the setting of preexcited AVNRT).
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