Ablation of Atrioventricular Junctional Tachycardias: Atrioventricular Nodal Reentry, Variants, and Focal Junctional Tachycardia

Introduction

Atrioventricular nodal reentrant tachycardia (AVRNT) is the most common form of paroxysmal supraventricular tachycardia (PSVT). It occurs more frequently in women than in men, and the initial episode of tachycardia tends to occur at an older age than in patients with atrioventricular (AV) reentrant tachycardia. Patients frequently complain of regular rapid pounding in the neck due to almost simultaneous atrial and ventricular contractions. A review of 500 consecutive patients studied in the authors’ laboratory revealed a mean age of 47 ± 15 years (range, 16–87 years); 367 (73%) of these patients were females. Twenty-two patients (4.4%) presented with syncope. In 11 (2.2%), sustained AVNRT was induced during an electrophysiology study performed to investigate the cause of syncope. Syncope did not recur after elimination of the arrhythmia.

Most patients with AVNRT present with a narrow complex tachycardia and no visible P wave or with a P wave at the end of the QRS (pseudo-r′ in V ₁ or pseudo-S in II, III, aV _F ) simulating an incomplete right bundle branch block ( Fig. 21.1 ). However, the patient may have a preexisting bundle branch block ( Fig. 21.2 ) or develop a functional bundle branch block due to fast rates that are then maintained by the linking phenomenon. Rate-dependent aberrancy can occur in both the right and the left bundle branches. There are electrocardiographic (ECG) features that suggest AVNRT as follows: (a) pseudo s wave in inferior leads and/or pseudo r’ wave in V1; (b) notch in aVL; (c) no retrograde P waves visible during tachycardia; and (d) pseudo r’ wave in lead aVR; (e) notch in lead 1. The presence of pseudo-r’ in lead aVR appears to be more accurate than other ECG criteria in one study.

Although most patients have no evidence of structural heart disease, AVNRT can also occur in patients with congenital or acquired heart disease. For example, in patients with an implantable cardiac defibrillator, AVNRT can result in inappropriate implantable cardioverter defibrillator therapies ( Fig. 21.3 ). Although a regular tachycardia is the most frequent presentation of AVNRT, some patients develop a regularly irregular tachycardia due to alternating antegrade or retrograde conduction through different slow AV nodal pathways. Even though the rhythm may appear irregular and resemble other arrhythmias, close inspection reveals that the short and long cycle lengths altersnate on a consistent basis ( Figs. 21.4 and 21.5 ). Although AVNRT can have a benign course, it can also result in disabling symptoms, especially in elderly patients in whom syncope may be the initial presentation. In addition, patients with AVNRT and coexisting intraventricular conduction disease may develop paroxysmal AV block due to the fast atrial rates ( Fig. 21.6 ).

Catheter ablation eliminates AVNRT in most patients with a low risk of complications. Therefore it can be offered as a first-line therapy to symptomatic patients and to those who cannot tolerate or do not wish to take antiarrhythmic agents. In addition, patients with high-risk occupations may undergo catheter ablation as first-line therapy. This chapter focuses on the electrophysiology, diagnosis, and ablation of AVNRT and its variants. All forms of AV nodal reentry can be treated by a combined anatomic and electrogram-guided approach, to guide a safe and successful ablation.

Anatomy of the Atrioventricular Node and its Inputs

The anatomy of the AV node and its relationship with nearby atrial structures and with the His bundle were described in great detail by Tawara. The AV node is not a right-sided structure as depicted in most textbooks but is indeed a septal structure located in the AV septum that separated the left ventricle from the right atrium. It is in contact with both the right and the left atria. The AV node is not insulated from the surrounding myocardium as it occurs with the His bundle or the right bundle branch. Right-sided and left-sided inputs provide activation to the AV node proceeding from both atria. Histologically, the AV node is a discrete structure that can be traced in consecutive sections. It is constituted by specialized myocardium with characteristic immunohistochemistry expressing HCN ₄ , which is the major isoform of the funny channel. The compact AV node is located at the apex of the triangle of Koch. This triangle is bounded by the tendon of Todaro posteriorly, the ostium of the coronary sinus (CS os) inferiorly, and the septal leaflet of the tricuspid valve anteriorly. However, AV nodal tissue extends well beyond the compact AV node. AV nodal conduction is modulated by the sympathetic and parasympathetic nervous system. Therefore the ability to demonstrate fast and slow AV nodal pathways in the antegrade and retrograde directions varies depending on the autonomic tone. The right coronary artery provides the AV nodal artery in 90% of patients and may run in the subendocardium close to the CS os, which may explain the rare instances of AV nodal block during radiofrequency (RF) ablation in the area of the slow pathway, despite considerable distance from the compact AV node.

Pathophysiology

The fundamental studies by Gaskell, His, and Tawara a century ago form the basis for the present understanding of the anatomy and physiology of the AV node. Mines, in 1913, was the first to describe the existence of two regions in the specialized conduction system with different conduction and recovery properties. Moe and associates later demonstrated the existence of two AV nodal pathways underlying AVNRT. The fast AV nodal pathway (β pathway) was found to have a longer refractory period than the slow AV nodal pathway (α pathway). These different electrophysiologic properties facilitate the onset and maintenance of AVNRT. Mendez and Moe found that the two AV nodal pathways located in the upper portion of the AV node in the rabbit communicated with a final lower common pathway. Denes and associates were the first to document the presence of dual AV nodal pathways in patients with and without AVNRT. The initial reported prevalence (10%) of dual AV nodal pathways is low compared with present-day findings, probably because electrophysiology studies were initially performed without sedation and therefore under a predominant adrenergic tone. Now under sedation, dual AV nodal pathways are found in most patients, even in those without AVNRT. Dual AV nodal pathways can be uncovered using a single atrial extrastimulus of increasing prematurity ( Fig. 21.7 ) or during decremental atrial stimulation. A 50 ms jump in the atrium–His bundle (AH) interval, following a premature atrial extrastimulus, is considered the hallmark of dual AV nodal physiology. Nevertheless, the lack of a jump does not rule out the existence of two distinct AV nodal pathways. In this regard, a continuous AV nodal conduction curve is observed in a subgroup of individuals with inducible AVNRT.

Dual AV nodal physiology is a normal behavior of the human AV node. The response of the AV node to premature stimulation and to different cycle lengths indicates the presence of two or more populations of AV nodal or perinodal cells with different refractoriness and conduction times. As mentioned previously, the presence of dual AV nodal physiology in itself does not imply the presence of AVNRT. A common misconception is to look for dual AV nodal physiology when AVNRT is suspected and to search for another arrhythmia when a jump is not observed. This simplistic approach can prevent identification of the correct mechanism of the arrhythmia. Consistent with these observations, similar incidences of dual AV nodal physiology in patients with and without AVNRT were found. A jump of 50 ms or longer was present in 83% (417 of 500) of patients with AVNRT and in 77% (385 of 500) of patients without AVNRT (studied for other reasons); this difference was not statistically significant. The magnitude of the jump, however, was greater in patients with AVNRT (93 ± 7 vs. 61 ± 7 ms, P < .05). If dual AV nodal pathways are present in most individuals with or without AVNRT, what is required to induce AVNRT? One explanation may be the fact that the slow AV nodal pathways are slower in patients with AVNRT, as reflected by a greater jump in those with clinical arrhythmia. This may represent an increase of collagen with age, which is supported by experimental studies that facilitate the induction of AVNRT by creating lesions that prevent antegrade activation by the superior approach to the AV node in dogs. A longer conduction time over the antegrade slow pathway allows recovery of excitability of the retrograde limb (fast or slow AV nodal pathway). Anatomic differences may be important because a larger CS os is observed in most patients with AVNRT ( Fig. 21.8 ) and may allow for greater conduction time over the slow pathway.

In fact, the proximal CS is significantly larger in patients with AVNRT than those with AVRT (14.1 ± 5 vs. 9.9 ± 2 mm, P < .0001). A cut off of proximal CS greater than 11.2 mm identifies AVNRT with a sensitivity of 92.6% and specificity of 76.9%.

The frequency of premature atrial or ventricular beats and the length of the excitable gap also modulate the frequency and duration of AVNRT. Finally, the coexistence of AVNRT with other arrhythmias, as well as occurrence of familial forms of AVNRT, suggests the possibility of an underlying abnormality.

Disagreement still exists regarding the nature and location of the slow and fast AV nodal pathways. The original mechanism that was advanced to explain this arrhythmia, is that these pathways represent longitudinal dissociation of conduction within the AV node itself. The most recent concept is that they represent different inputs to the AV node. Before the advent of surgical and catheter ablation, the slow and fast AV nodal pathways were believed to be part of the AV node, representing regions with different electrophysiologic properties (i.e., longitudinal dissociation). In fact, several experimental and clinical observations supported an intranodal location of these AV nodal pathways and the reentrant circuit supporting AVNRT. In some patients with AVNRT, atrial activation close to the AV node can be dissociated from the reentrant circuit without interruption of the tachycardia ( Fig. 21.9 ). This observation suggests that reentry confined to the AV node can sustain AVNRT without atrial involvement. Different degrees of ventriculoatrial (VA) block during AVNRT occur in the upper common pathway, allowing continuation of the tachycardia without retrograde atrial activation. In a similar fashion, the His–Purkinje system and the ventricles are not part of the reentrant circuit. This is demonstrated by episodes of 2:1 AV block with persistence of AVNRT ( Fig. 21.10 ). Block can occur either proximal or distal to His bundle activation. This block is functional and occurs in tachycardias with short cycle lengths, which find the His–Purkinje system refractory. As mentioned before, the presence of concurrent intraventricular conduction abnormalities may even result in paroxysmal AV block during AVNRT (see Fig. 21.6 ).

Earliest atrial activation during retrograde AV nodal conduction can occur in the upper or lower portion of the triangle of Koch, depending on whether the fast or the slow AV nodal pathway is activated. These observations and the results of surgical and catheter ablation of the anterior (superior) or posterior (inferior) approaches to the AV node led to the conclusions that the fast and slow AV nodal pathways have an extranodal component and that the atrium is required to sustain AVNRT. However, the portion of the atrium that is involved in the reentrant circuit remains elusive.

The original description of the AV node, made by Tawara in 1906, included posterior extensions of the AV node reaching both the mitral and tricuspid annuli. These observations were later confirmed by Becker, Inoue, and Anderson ( Fig. 21.11 ). More recently, we demonstrated the presence of a left atrial input to the AV node proceeding from the mitral annulus. This left atrial input to the AV node represents the electrophysiologic counterpart of the leftward extension of the AV node. Therefore in addition to the right-sided superior (anterior) and inferior (posterior) inputs to the AV node, the mitral annulus provides an independent input for activation proceeding from the left atrium (see Fig. 21.11 ). These inputs probably participate in the various forms of AVNRT by providing entrance and exit sites in a reentry that involves the atrium, or they may represent exit points from an intranodal circuit sustaining AVNRT. VA conduction over the slow pathway has been shown to result in earliest atrial activation on the left side of the interatrial septum, which is abolished with ablation of the slow pathway in the right atrium. Consistent with the clinical observation of intranodal reentry, different forms of AVNRT can be contained within the transitional cells of the posterior AV nodal input in a rabbit heart, owing to functional dissociation of cellular activation. Fig. 21.12 depicts possible reentrant circuits that are either contained in the compact AV node or involve the right- and left-sided inputs. As can be observed, there are multiple possible reentrant loops. Identifying the reentrant mechanism in a given patient can be difficult even with entrainment maneuvers.

Diagnosis

Three main forms of AVNRT are observed: slow–fast, slow–slow, and fast–slow AVNRT. In a single patient, one, two, or all three forms may be present at different times during the electrophysiology study. There is no electrophysiologic finding that alone is diagnostic of AVNRT; the diagnosis is made on the weight of typical features and the exclusion of atrial tachycardias, junctional tachycardia (JT), and septal accessory AV pathways using entrainment maneuvers. Electrophysiologic variables of different forms of AV nodal reentry are given in Table 21.1 .

An initial careful baseline electrophysiologic study is required before any ablation procedure. This is especially relevant for AVNRT because other supraventricular or ventricular arrhythmias may mimic this arrhythmia or coexist. The presence of a concealed accessory AV pathway should be ruled out before induction of the tachycardia by performing para-Hisian and differential ventricular pacing.

The electrophysiology study will demonstrate dual AV nodal physiology in approximately 85% of patients with AVNRT, but dual AV nodal physiology can also be observed in patients without AVNRT. Conversely, the absence of verifiable dual AV nodal physiology does not rule out AVNRT. The diagnostic criteria for dual AV nodal physiology are listed in Box 21.1 . Prolongation of the AH interval to more than 180 ms during decremental atrial pacing is usually indicative of conduction over the slow pathway. This frequently manifests as a paced PR interval greater than the PP interval such that the paced atrial depolarization conducts, not to the next QRS, but to the second QRS following the pacing stimulus ( Fig. 21.13 ).

It has recently been stated that coronary sinus pacing can initiate AVNRT with a shorter critical AH interval compared with pacing from the right atrium. However, coronary sinus pacing is known to result in a shorter A H interval than right atrial pacing. This is because coronary sinus stimulation will depolarize the AV node via the left atrial input and also because the A H interval is dependent not only on AV nodal conduction but also on how activation reaches the AV node and how the atrium is close to the node.

During atrial extrastimulus testing, dual AV nodal physiology is typically manifested by a jump of 50 ms or longer in the A2H2 interval following a shortening in the A1A2 interval by 10 ms (see Fig. 21.7 ). When two atrial extrastimuli are delivered, a jump from fast to slow-pathway conduction is defined as an increase in the A3H3 interval of 50 ms or more in response to a decrement of 10 ms in the A2A3 interval (A1A2 being constant). The induction of AV nodal echo beats is an indication of dual AV nodal physiology. The diagnosis of retrograde dual AV nodal physiology is made based on jumps but is mainly dependent on changes of earliest atrial activation site ( Box 21.2 ). Retrograde His bundle–atrial (HA) interval jumps, and retrograde slow, antegrade fast AV nodal echo beats, may be seen. In addition, a change in the site of earliest retrograde atrial activation from near the His bundle area to the proximal CS region indicates a transition from retrograde fast pathway to retrograde slow-pathway conduction.

Induction of AVNRT is dependent on achieving a critical AH interval for typical slow–fast AVNRT; this requires exclusive antegrade slow-pathway conduction, which can be achieved by atrial extrastimulus testing or atrial burst pacing near the Wenckebach cycle length. If antegrade slow-pathway conduction cannot be achieved because short antegrade fast-pathway refractoriness, S ₃ stimulation, burst atrial pacing, or ventricular stimulation with or without isoproterenol may be required. If retrograde fast-pathway conduction is absent during ventricular pacing (VA block or earliest retrograde atrial activation at proximal CS) or by lack of echoes or AVNRT following antegrade slow-pathway conduction, isoproterenol infusion should be given. It is important to remember that retrograde block over the fast AV nodal pathway may be due to mechanical trauma of the fast pathway by the catheter recording His bundle activity, which can be minimized by advancing the catheter to the ventricle.

Slow–Fast Variant

The typical form, or slow–fast variant, occurred in 414 (83%) of 500 patients studied at the authors’ institution. Slow–fast AVNRT can be associated with other forms of AVNRT. For example, 3.5% of patients also had slow–slow AVNRT, 2% had fast–slow AVNRT, and in 1%, the three forms coexisted in the same patient.

The electrocardiogram obtained during tachycardia can suggest the diagnosis when the retrograde P wave is superimposed on the terminal portion of the QRS, giving rise to a pseudo-right bundle branch block pattern ( Fig. 21.14 ). As mentioned before, although most patients have a normal QRS, slow–fast AVNRT can also occur in patients with a wide QRS due to preexisting bundle branch block or rate-dependent functional AV block (see Fig. 21.2 ). The tachycardia cycle length (TCL) averaged 361 ± 59 ms in our patients (range, 235–660 ms).

The antegrade limb of the tachycardia is the slow AV nodal pathway, with an AH interval longer than 180 ms (range, 190–545 ms; mean, 312 ± 61 ms; see Table 21.1 ). A short VA (measured from the surface QRS to the earliest intracardiac atrial electrogram) time of less than 60 ms excludes reciprocating tachycardias using a concealed accessory pathway. However, atrial tachycardias with 1:1 AV conduction over the slow AV nodal pathway can have a short VA time, simulating AVNRT. The VA relationship during atrial tachycardia may change over time depending on the autonomic tone and facilitate the differential diagnosis. Induction of slow–fast AVNRT is usually accomplished by atrial extrastimuli or rapid atrial stimulation. Adrenergic stimulation (isoproterenol, 1–4 μg per minute) may be needed. Inducibility of AVNRT sometimes occurs only after the infusion of isoproterenol has been discontinued. Occasionally, atropine, 1 to 2 mg, with or without catecholamine infusion is necessary for AVNRT induction. Regardless of the maneuver used, induction of slow–fast AVNRT from the atrium requires antegrade block over the fast AV nodal pathway, with antegrade conduction over the slow AV nodal pathway allowing retrograde conduction over the fast AV nodal pathway. Less commonly, ventricular stimulation can also induce slow–fast AVNRT. Local atrial activation near the exit site of the fast AV nodal pathway (superior aspect of the triangle of Koch) can be recorded using closely spaced electrodes (see Fig. 21.15 and Fig. 21.16 ). The site of earliest retrograde atrial activation is critical to differentiate slow–fast from slow–slow AVNRT because the HA intervals can overlap in these two forms of tachycardia. In the studied population, the HA interval in the slow–fast form was 45 ± 11 ms (range, 25–145 ms). A contemporary conceptualization of the reentry circuit for slow–fast AVNRT is shown in Fig. 21.12C . In this model, retrograde atrial activation through the fast pathway activates both the left and right sides of the atrial septum. The wave front of right atrial activation fails to penetrate into the triangle of Koch because of block along the Eustachian ridge. The left atrial wave front, however, activates the CS myocardium and propagates to the CS os and inferior triangle of Koch between the os and the tricuspid valve. The wave front then ascends the atrial septum in the triangle of Koch to activate the fast pathway and complete the circuit. In this conceptualization, the right inferior extension comprises the anterograde slow pathway, and the fibers crossing the superior tendon of Todaro comprise the retrograde fast pathway. Ablation within the CS or left atrium is necessary when the left inferior extension or left atrial myocardium provides the critical portion to the reentry circuit rather than the right inferior extension.

The response after ventricular overdrive pacing is an additional maneuver to support the diagnosis of AVNRT. During ventricular pacing with 1:1 V-A conduction and atrial entrainment, the VA interval is more than 85 ms longer than the corresponding VA interval during tachycardia. Upon cessation of ventricular pacing with tachycardia continuation, a VAV, ventricular-atrial-ventricular response is noted. In addition, the difference between the ventricular postpacing interval (PPI) and TCL is more than 115 ms. Correction of the PPI may be needed to account for rate-related prolongation of the return AH interval—Δ = [PPI – (AH return – AH supraventricular tachycardia) – TCL] ( Fig. 21.17 ). The HA interval is typically stable during tachycardia and after pacing maneuvers.

To some extent, it is possible to dissociate both the atrium and the ventricle from the tachycardia. However, atrial or ventricular preexcitation will eventually advance AVNRT if His bundle activation is altered. AV block, either distal to His, or between the His and lower common pathway, is sometimes seen at the onset of tachycardia. Late ventricular extrastimuli introduced during His refractoriness will not perturb AVNRT, but those that are able to advance retrograde His bundle activation will preexcite the atrium and entrain the tachycardia.