Atrioventricular Nodal Reentrant Tachycardia
Atrioventricular nodal reentrant tachycardia (AVNRT) represents the most common regular supraventricular arrhythmia in humans.1 The precise anatomic site and nature of the pathways involved have not yet been established, and several attempts to provide a reasonable hypothesis based on anatomic or anisotropic models have been made.2 There has been considerable evidence that the right and left inferior extensions of the human atrioventricular (AV) node and the atrionodal inputs they facilitate may provide the anatomic substrate of the slow pathway, and a comprehensive model of the tachycardia circuit for all forms of AVNRT based on the concept of atrionodal inputs has been proposed.2 Still, however, the circuit of AVNRT remains elusive. Recently, time-honored conventional schemes for the diagnosis and classification of the various forms of the arrhythmia have been refuted in part by evolving evidence. Recognition of the various types of AVNRT is important, however, to expedite diagnosis and allow implementation of appropriate ablation therapy without complications. We present an update on AVNRT with a particular emphasis on electrophysiological criteria used for the differential diagnosis of regular, supraventricular tachycardias.
Typically, AVNRT is a narrow-complex tachycardia, ie, QRS duration <120 ms, unless aberrant conduction, which is usually of the right bundle-branch type, or a previous conduction defect exists. Tachycardia-related ST depression and RR-interval variation may be seen. RR alternans in AVNRT has been attributed to the proposed model of a figure of 8 reentry with continuous crossing over of antegrade activation through an inferior input to the contralateral superior input via the node.2
In the typical form of AVNRT (slow-fast), abnormal (retrograde) P′ waves are constantly related to the QRS and in the majority of cases are indiscernible or very close to the QRS complex (RP′/RR <0.5). Thus, P′ waves are either masked by the QRS complex or seen as a small terminal P′ wave that is not present during sinus rhythm (Figure 1). In the atypical form of AVNRT (fast-slow), P′ waves are clearly visible before the QRS, ie, RP′/P′R >0.75 (Figure 2), denoting a “long RP tachycardia,” and are negative in leads II, III, aVF, and V6 but positive in V1. P′ waves are shallow in the inferior leads in the rare form of anterior fast-slow AVNRT.3 Although AV dissociation is usually not seen, it can occur because neither the atria or the ventricles are necessary for the reentry circuit. If the tachycardia is initiated by atrial ectopic beats, the initial (ectopic) P′ wave usually differs from the subsequent (retrograde) P′ waves (Figure 1).
Electrophysiological Classification of AVNRT Types
The recognition of the fact that AVNRT may present with atypical retrograde atrial activation has made diagnosis of the arrhythmia and classification attempts more complicated. Electrophysiological behavior compatible with multiple pathways may also be seen,4 and in some patients, several forms of AVNRT may be inducible at electrophysiology study.3,5 Heterogeneity of both fast- and slow-conduction patterns has been well described, and all forms of AVNRT may display anterior, posterior, and middle retrograde activation patterns (Table).4,5–7 In certain cases of atypical AVNRT, retrograde atrial activation is even suggestive of a left lateral accessory pathway.8–10 Appropriate diagnosis in this setting is of importance for the avoidance of prolonged procedures with high fluoroscopy times and unnecessary radiofrequency lesions.11
In the slow-fast form of AVNRT, the onset of atrial activation appears before, at the onset, or just after the QRS complex, thus maintaining an atrial-His/His-atrial ratio (AH/HA) >1. Although typically, the earliest retrograde atrial activation is recorded at the His bundle electrogram, careful mapping studies have demonstrated that posterior or even left septal fast pathways may occur in up to 7.6% of patients with typical AVNRT.4,6,7,12,13 The possibility of a bystander atrionodal pathway12 cannot be ruled out in all cases, but studies of left septal mapping indicate that if left septal His recordings were routinely performed in patients with AVNRT, left-sided retrograde fast pathways would be documented in a considerable proportion of patients studied (Figure 3).14
In the fast-slow form of AVNRT (≈5% to 10% of all AVNRT cases), retrograde atrial electrograms begin well after ventricular activation, with an AH/HA ratio <1, which indicates that retrograde conduction is slower than antegrade conduction. The VA interval, measured from the onset of ventricular activation on the surface ECG to the earliest deflection of the atrial activation in the His bundle electrogram, is >60 ms, and in the high right atrium, it is >100 ms.1 Earliest retrograde atrial activation is traditionally reported at the base of the triangle of Koch, near the coronary sinus ostium.1 Detailed mapping of retrograde atrial activation in large series of patients, however, has produced variable results, with eccentric atrial activation at the lower septum or even the distal coronary sinus.5–8 Left septal mapping studies have also provided evidence of left-sided earliest retrograde atrial activation during retrograde slow-pathway conduction (Figure 4).15 Thus, fast-slow AVNRT may be of the posterior, anterior, or middle type according to the mapped location of the retrograde slow pathway.5
In the slow-slow form, the AH/HA ratio is >1 but the VA interval is >60 ms, which suggests that 2 slow pathways are used for both anterograde and retrograde activation. Earliest retrograde atrial activation is usually at the coronary sinus ostium,16 but variants of left-sided atrial retrograde activation (distal coronary sinus) have also been reported.9,10 The so-called posterior or type B AVNRT has been demonstrated in approximately 2% of patients with slow-fast AVNRT; VA times are prolonged, but the AH/HA ratio remains >1.17 Thus, it appears that the reported cases of posterior slow-fast AVNRT may actually represent the slow-slow form.
In the presence of a narrow-QRS tachycardia, AVNRT should be differentiated from atrial tachycardia or orthodromic AV reentrant tachycardia (AVRT) due to an accessory pathway. When a wide-QRS tachycardia is encountered and ventricular tachycardia is excluded, the possible diagnoses are AVNRT or atrial tachycardia with aberrant conduction due to bundle-branch block, AVNRT with a bystander accessory pathway, and antidromic AVRT due to an accessory pathway. Aberrant conduction, although rare, can be seen in AVNRT and is usually of the right bundle-branch type; however, cases of left bundle-branch block have been reported.
AVNRT Versus Atrial Tachycardia
Differential diagnosis may be difficult particularly with peri-AV nodal atrial tachycardias that, when reentrant, usually respond to adenosine and verapamil.17a
Exclusion of an atrial tachycardia on the 12-lead ECG is difficult, and pacing maneuvers are necessary for this purpose.
The demonstration of a constant His-atrial interval of the return cycle after introduction of a premature atrial impulse with a wide range of coupling intervals during tachycardia makes the diagnosis of atrial tachycardia unlikely. In particular, the difference in the AH interval between atrial pacing and the tachycardia is >40 ms in AVNRT but <10 ms in atrial tachycardia.18 Differential atrial overdrive pacing from the high right atrium and the coronary sinus has also been proposed for diagnosis of atrial tachycardia versus slow-fast AVNRT and AVRT. A difference of >10 ms in the first V-A time after atrial overdrive from the high right atrium and the coronary sinus suggests atrial tachycardia.19
Tachycardia termination by a ventricular extrastimulus that did not conduct to the atrium indicates an origin other than atrial tachycardia. A useful criterion is the atrial response on cessation of ventricular pacing associated with 1:1 ventriculoatrial conduction during tachycardia. Atrial tachycardia is associated with an A-A-V response, whereas AVNRT or AVRT produces an A-V response.20 This rule, however, has many exceptions. The His deflection should be considered in this respect, because a late V electrogram might give an apparent A-A-V response that is actually an A-H-A-V response in the presence of AVNRT or AVRT, as opposed to A-A-H-V in the presence of atrial tachycardia.21 Apart from a long HV interval during slow-fast AVNRT that may cause atrial activation to precede ventricular activation, a very long AH interval that exceeds the tachycardia cycle length may also produce a pseudo A-A-V response.22 A pseudo A-V response can also be seen with isoprenaline-increased automaticity of the AV junction in the sense that junctional activity precludes conduction of the second A of the A-A-V response to the ventricle.23
AVNRT Versus AVRT Due to Septal Accessory Pathways
AVNRT may display eccentric atrial activation, and septal pathways may have decremental conduction properties and concentric atrial activation, thus making the differential diagnosis challenging.
In the case of relatively delayed retrograde conduction that allows the identification of retrograde P waves, ECG criteria can be applied for diagnosis. The presence of a pseudo r′ wave in lead V1 or a pseudo S wave in leads II, III, and aVF has been reported to indicate anterior AVNRT with an accuracy of 100%. A difference of >20 ms in RP intervals in leads V1 and III was indicative of posterior AVNRT rather than AVRT due to a posteroseptal pathway.24 The documentation of preexcited beats, AV dissociation, and the induction of bundle-branch block during tachycardia may assist the differential diagnosis. AV block or AV dissociation, although uncommon and short-lasting, may be seen in AVNRT and excludes the presence of an accessory pathway.1 Similarly, the development of bundle-branch block either spontaneously or after introduction of ventricular extrastimuli during AVNRT does not change the AA or HH intervals. A significant change in the VA interval with the development of bundle-branch block is diagnostic of orthodromic AVRT and localizes the pathway to the same side as the block.1
The difference in the AH interval between atrial pacing and the tachycardia may allow differentiation of atypical AVNRT from other types of long RP′ tachycardias. A ΔAH >40 ms has been reported to indicate AVNRT, whereas in patients with AVRT due to septal pathways or atrial tachycardia, these differences were <20 and 10 ms, respectively.18
His-Synchronous Ventricular Extrastimulation
In the presence of septal decremental pathways, ventricular extrastimuli introduced while the His bundle is refractory during tachycardia (ie, delivered coincident with the His potential or up to 50 ms before this) may advance or delay subsequent atrial activation (extranodal capture). In AVNRT, atrial activity is not perturbed with His-synchronous ventricular extrastimulation. Failure to reset the atria suggests but does not prove that an accessory pathway is not present or that it is relatively far from the site of premature stimulation. Demonstration of resetting excludes AVNRT if extrastimuli are delivered very close to inferior nodal extensions.25
Atrial and ventricular conduction starts almost simultaneously in AVNRT, and VA times during tachycardia are therefore shorter than during ventricular pacing. The difference between the tachycardia cycle length and the longest premature ventricular stimulation interval at which atrial capture occurs during tachycardia defines the so-called preexcitation index.26 A preexcitation index of 100 ms or more characterizes AVΝRT, whereas an index less than 45 ms characterizes AVRT with a septal pathway. Consideration of the ratio between the minimum ventriculoatrial interval during tachycardia and during ventricular pacing in sinus rhythm is more practical. Ratios of 0.32 to 0.27 indicate AVNRT, 0.91 to 1.08 indicate AVRT with a posteroseptal pathway, and 0.94 to 1.29 indicate AVRT with an anteroseptal pathway.27 A difference in the VA interval during tachycardia and apical right ventricular (RV) pacing >90 ms has been reported to differentiate patients with AVNRT from those with AVRT.28 VA times obtained by apical RV pacing can be misleading in the case of multiple accessory pathways or simultaneous nodal and accessory pathway retrograde conduction. The difference between the ventriculoatrial interval obtained during apical pacing and that obtained during posterobasal pacing has been found to discriminate between patients with posteroseptal pathways (>10 ms) and those with nodal retrograde conduction (<5 ms).29 Parahisian pacing during sinus rhythm and the change in timing and sequence of retrograde atrial activation between His and proximal right bundle-branch capture and noncapture have also been used for differentiation between AV nodal and septal pathway retrograde conduction.30 The response is considered extranodal when the retrograde atrial activation during His bundle capture is the same as during ventricular capture without His bundle capture. Parahisian pacing techniques are cumbersome and may not be possible in up to 50% of tachycardia cases that are studied.31
The demonstration of a V-H-A response at ventricular stimulation that is performed during sinus rhythm indicates retrograde conduction through the AV node and has been used to differentiate atypical AVNRT from AVRT.32 However, a V-H-A pattern cannot rule out a fast-slow AVNRT, and an accessory pathway with conduction slower than that of the AV node may produce a V-H-A pattern. Recently, the induction of retrograde right bundle-branch type (defined as an increase of the VH interval >50 ms) by ventricular extrastimulation during tachycardia has been proposed for differential diagnosis purposes.31 Similar increases in the VH and VA intervals indicated retrograde AV nodal conduction, whereas a VH interval change that exceeded that of the VA interval indicated the presence of an accessory pathway because it bypassed the decremental conduction system. This maneuver provides very high sensitivity and specificity (almost 100%) but requires recording of retrograde His bundle activation.
The difference between HA intervals during pacing and during tachycardia (ΔHA) has also been used. In a study of 84 patients, a retrograde His bundle deflection was present in 93% of them, and the ΔHA was >0 ms in AVNRT and less than −27 ms in orthodromic AVRT that incorporated a septal accessory pathway. Thus, an intermediate value of ΔHA=−10 ms had 100% sensitivity, specificity, and predictive accuracy in differentiating the 2 forms of tachycardia.33
The use of tachycardia entrainment via ventricular pacing for differential diagnosis of supraventricular tachycardias was introduced by Ormaetxe et al.34 Right apical stimulation is relatively close to the insertion of a septal accessory pathway as opposed to the AV junction; thus, ventricular fusion during resetting or entrainment of tachycardia has been reported to occur in patients with AVRT due to septal pathways but not with AVNRT.34 Michaud et al35 have proposed 2 additional criteria for differential diagnosis. The ventriculoatrial (VA) interval and tachycardia cycle length (TCL) were measured during tachycardia, and entrainment of the tachycardia was accomplished with RV apical pacing. The intervals between the last ventricular pacing stimulus and the last entrained atrial depolarization during tachycardia (SA), as well as the postpacing interval (PPI), were considered. All patients with AVNRT had SA-VA intervals >85 ms and PPI-TCL intervals >114 ms. The SA-VA and PPI-TCL criteria should be valid regardless of the type of AVNRT (slow-fast or fast-slow). However, conventional entrainment techniques do not take into account pacing-induced incremental AV nodal conduction (ie, in the postpacing A-H) that may alter the PPI. Thus, González-Torrecilla et al36 “corrected” the PPI-TCL difference by subtracting from it the difference of postpacing AH interval minus basic AH interval. The presence of a corrected PPI-TCL <110 ms indicated AVRT. Entrainment through basal RV pacing away from the septum may produce prolonged PPI-TCL intervals in the absence of a septal pathway owing to the distance of the RV base from the AV node (activation occurs retrogradely through the distal His-Purkinje system) and has been found to be superior to apical entrainment for diagnostic purposes.37 Recently, differential entrainment from the apex or the basal area of the RV was investigated.38 A differential (between base and apex) corrected PPI-TCL >30 ms or a differential VA interval >20 ms predicted AVNRT very reliably (Figure 5). The main advantage of this technique is that the differential VA interval could be calculated from the last paced beat in case the tachycardia was terminated after transient entrainment.
The comparison of HA interval during tachycardia and during entrainment from the RV apex or near the His bundle to obtain a recordable retrograde His bundle deflection has also been used for differentiation of AVNRT from AVRT. Positive ΔHA (HA during entrainment minus HA during SVT) indicates AVNRT, whereas negative ΔHA indicates the presence of an accessory pathway.39
Parahisian entrainment that considered the difference in stimulus to earliest retrograde atrial activation during His and both RV and His capture has also been reported.40 Assessment of the SA-VA and PPI-TCL intervals by parahisian entrainment may assist in differentiation between slow-fast AVNRT and AVRT, but the cutoff values are lower than that obtained with RV apical pacing (75 and 100 ms, respectively), presumably owing to conduction through the septum.41 These techniques are rather cumbersome, requiring differential capture and both recording and identification of retrograde His and local ventricular potentials.
In many studies, proposed criteria have been examined in patients with typical slow-fast AVNRT; their effectiveness in differentiating between fast-slow AVNRT and decremental accessory pathways has not been tested. In clinical practice, pacing or other maneuvers cannot be applied in all cases, and multiple criteria must be used for the differential diagnosis of narrow-complex tachycardias with atypical characteristics.42
AVNRT With Bystanding Accessory Pathways Versus Antidromic AVRT
Antidromic AVRT, ie, tachycardia that uses the accessory pathway for antegrade conduction and the AV node for retrograde conduction, may be induced in approximately 6% of patients with accessory pathways located in the left or right free wall or the anterior septum at an adequate distance from the AV node.1 Mahaim atriofascicular pathways may give rise to AVRT or act as bystanders in AVNRT with left bundle-branch block morphology.
The possibility of AVNRT that is conducted over a bystander accessory pathway should be considered in the presence of transition from narrow- to wide-complex tachycardia of a similar cycle length and without disruption of the HH intervals.43 In this case, atrial extrastimuli fail to induce advancement of the following preexcited QRS complex, the next retrograde His bundle deflection where apparent, and the subsequent atrial deflection without changing the retrograde atrial activation sequence, as may happen in the presence of a macroreentrant loop (Figure 6). Although no extensive series have been published, application of entrainment criteria (SA-VA and PPI-TCL) from the apex44 or the apex and the base for differential entrainment45 is theoretically appealing and has been proposed to distinguish between antidromic AVRT and AVNRT with a bystander fiber.
AVNRT Versus Nonreentrant Junctional Tachycardias
Nonreentrant junctional tachycardias are rare but should be recognized, because catheter ablation conveys a higher risk of AV block than in AVNRT. Nonparoxysmal junctional tachycardia was frequently diagnosed in the past as a junctional rhythm of gradual onset and termination with a rate between 70 and 130 bpm and was considered a typical example of digitalis-induced delayed afterdepolarizations and triggered activity in the AV node.1 Presently, focal junctional tachycardia occurs as a congenital arrhythmia or early after infant open heart surgery, but it can also be seen in adult patients, and this tachycardia is associated with a structurally normal heart.46,47 Its cause is increased automaticity or triggered activity.47 The usual ECG finding is a narrow QRS tachycardia with AV dissociation. Occasionally, the tachycardia might be irregular, thus resembling atrial fibrillation. At electrophysiology study, there is a normal HV interval and normal AV conduction curves.46 The arrhythmia is not inducible by programmed electric stimulation but is sensitive to isoproterenol administration, and in some cases, rapid atrial or ventricular pacing may result in tachycardia induction. During tachycardia, there is a normal or increased HV interval with AV dissociation that is interrupted by frequent episodes of ventriculoatrial conduction, with earliest atrial activation in the posteroseptal, anteroseptal, or midseptal regions. At times, the mode of tachycardia induction resembles a double AV nodal response that is characteristic of AVNRT.47
The differentiation of AVNRT from junctional tachycardia is of clinical importance, because ablation of the latter is associated with an increased risk of AV block. A positive ΔHA interval (ie, HA during pacing from a basal site of the RV minus HA during tachycardia) has been reported to indicate junctional tachycardia. In a recent study, the average ΔHA interval in AVNRT was −10 ms, although positive values were encountered.48 Padanilam et al49 described the use of premature atrial stimuli for differential diagnosis of slow-fast AVNRT and nonreentrant junctional tachycardia. An atrial premature complex that is timed to His refractoriness and advances the His electrogram of the subsequent cycle indicates that anterograde slow-pathway conduction is involved and suggests the diagnosis of AVNRT. An atrial extrastimulus that advances the His potential immediately after it without terminating the tachycardia indicates that the retrograde fast pathway is not essential for the circuit and suggests the diagnosis of junctional tachycardia. If no dual (or multiple) response of the AV node is present, this criterion has a high specificity.
Nonreentrant AV nodal tachycardia caused by simultaneous multiple nodal pathway conduction is an uncommon mechanism of AV nodal tachycardia and has been associated with repetitive retrograde concealment or “linking” phenomena.50 These are expressed in the form of ventricular pauses with a consistent AV relationship after the pause.
In acute episodes of AVNRT that do not respond to Valsalva maneuvers, intravenous adenosine is the treatment of choice. Continuous administration of antiarrhythmic drugs may be ineffective in up to 70% of cases.51 Thus, catheter ablation is the current treatment of choice. Slow-pathway ablation or modification is effective in both typical and atypical AVNRT. Usually, a combined anatomic and mapping approach is used, with ablation lesions delivered at the inferior or mid part of the triangle of Koch either from the right or the left septal side.52 Multicomponent atrial electrograms or low-amplitude potentials, although not specific for identification of slow-pathway conduction, are used to successfully guide ablation at these areas. This approach is associated with a 0.5% to 1% risk of AV block and has a recurrence rate of approximately 4%. Advanced age is not a contraindication for slow pathway ablation.53 The preexistence of first-degree heart block may carry a higher risk for late AV block and slow pathway modification, as opposed to complete elimination, is probably preferable in this setting.54
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