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How to Perform Radiofrequency Ablation and Cryoablation for AV Nodal Reentrant Tachycardia

Paul J. Wang, MD; Zhongwei Cheng, MD; Scott R. Ceresnak, MD

Introduction

Atrioventricular nodal reentrant tachycardia (AVNRT) is the most common paroxysmal supraventricular tachycardia (SVT), affecting women twice as frequently as men.^1–3 Catheter-based radiofrequency (RF) ablation^1–23 and cryoablation^24–28 are now well established as the definitive treatments for most patients, with excellent success rates (> 90%–97% cure) and a low incidence of serious complications.^4,5 AVNRT typically occurs in patients with dual AV nodal physiology. The fast pathway is anteriorly situated along septal portion of the tricuspid annulus. The slow pathway is posteriorly situated close to the CS ostium. Discontinuous, nonuniform anisotropy within the triangle of Koch is a substrate that can support functional, anisotropic reentry, a condition that can exhibit dual-pathway physiological characteristics.

There are three types of AVNRT: slow-fast (SF), also called “typical”; fast-slow (FS) and slow-slow (SS) type. In the common or “typical” form of AVNRT, which accounts for about 90% of cases, the antegrade limb of the reentrant circuit usually conducts slowly, whereas the retrograde limb conduction is fast.

The two major energy sources used for AVNRT therapy include RF energy and cryoablation. Lesion formation with RF energy is more rapid, occurring within 30 seconds and resulting in junctional beats, which provide a marker of ablation. Cryoablation lesions are longer, usually 4 minutes in duration, but provide a safety margin of reversibility, essentially eliminating the risk of AV block.²

Preprocedural Preparation

There are very limited tests required before catheter ablation of AVNRT. It may be useful to have an echocardiogram to exclude any coexisting abnormalities of the tricuspid valve and annulus.

It is quite useful to have an ECG recording of the SVT, since in most cases the diagnosis of mechanism of the tachycardia is not known and an ECG of the rhythm may provide clues. Atrial activity 80 ms or less after the onset of the QRS complex is most consistent with AVNRT. There may a somewhat inverted P wave in the inferior leads and an rSr in lead V₁. Occasionally the P wave may be later after the termination of the QRS complex. In atypical AVNRT, the P wave is usually before the QRS complex. A P-wave morphology that is upright in the inferior leads effectively excludes AVNRT.

Having a recording of the SVT prior to the ablation procedure also provides a greater degree of certainty that a patient’s palpitations are not due to sinus tachycardia. If no SVT is induced during EP testing, the decision will need to be made how to proceed. Some electrophysiologists will perform an empiric ablation of the slow AV nodal pathway if the patient has dual AV nodal pathways and a documented SVT consistent with AVNRT despite the noninducibility of the tachycardia.

An ECG at the spontaneous initiation of the SVT is particularly helpful, since it provides a potential clue to the mechanism. An abrupt prolongation of the P-R interval with the first beat of the tachycardia would be highly suggestive of AVNRT as the mechanism. Similarly, spontaneous termination of the tachycardia may provide clues regarding the mechanism. Termination with a P wave that is not premature would be most consistent with an AVNRT or AV reciprocating tachycardia.

An important part of the AVNRT procedure is the baseline characterization of AV and VA conduction. Ventricular overdrive pacing and premature stimulation are used to characterize VA conduction and to exclude the existence of a retrograde conducting accessory pathway. In atypical AVNRT, ventricular stimulation may be needed for induction. Atrial overdrive pacing and atrial premature stimulation are performed to characterize AV conduction. The atrial drive cycle length at which AV Wenckebach occurs is determined. During atrial premature stimulation, the AV nodal effective refractory period is determined. Dual AV nodal pathways, usually defined as an increase in the A2-H2 interval of 50 ms or more for a 10- to 15-ms decrease in the A1-A2, is noted (Figure 6.1). In some cases, isoproterenol infusion, usually from 1 to 4 mcg per minute IV, is required to induce AVNRT. Double atrial stimuli in sinus rhythm sometimes may be more effective than atrial premature stimulation alone.

Moe et al⁶ was first to demonstrate the existence of 2 AV nodal pathways underlying AVNRT. The fast pathway was found to have a longer refractory period than the slow pathway. These different EP properties facilitate the onset and maintenance of AVNRT. Dual AV nodal physiology is a normal behavior of the human AV node. The presence of dual AV nodal physiology in itself does not imply the presence of AVNRT. Table 6.1 summarizes the diagnostic criteria for dual AV nodal physiology.

Three main forms of AVNRT are found: slow-fast, slow-slow, and fast-slow AVNRT. There is no EP finding that alone is diagnostic of AVNRT; the diagnosis is made based on the typical features and the exclusion of atrial tachycardias, junctional tachycardia, and septal accessory AV pathways. Table 6.2 summarizes the diagnostic criteria of AVNRT and left-sided variants.

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 or atrial burst pacing near the Wenckebach cycle length. If antegrade slow pathway conduction cannot be achieved because short antegrade fast pathway refractoriness, S3 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.

The ECG obtained during tachycardia can suggest the diagnosis when the retrograde P wave is superimposed on the terminal portion of the QRS. The antegrade limb of the tachycardia is the slow pathway, with an A-H interval longer than 180 ms. A short V-A (measured from the surface QRS to the earliest intracardiac atrial electrogram) time of < 60 ms excludes the concealed accessory pathway tachycardias.7 Adrenergic stimulation (isoproterenol, 1–4 mcg/min) may be used for AVNRT induction. 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. The site of earliest retrograde atrial activation is critical to differentiate slow-fast from slow-slow AVNRT. About 6% of patients demonstrate early retrograde atrial activation in the CS (so-called eccentric atrial activation) because of muscular connections between the LA and the CS.⁸

Slow-Slow

In this form of reentry, a slow AV nodal pathway is used as the antegrade limb and another slow AV nodal pathway as the retrograde limb. The ECG during tachycardia may show characteristic negative P waves in the inferior and precordial leads, typical of earliest retrograde atrial activation in the proximal CS. This tachycardia can be induced by atrial or ventricular stimulation and frequently requires administration of isoproterenol. The earliest site of retrograde atrial activation is typically found near the anterior edge of the CS ostium or just inside the CS. The earliest site of retrograde atrial activation near the CS ostium is what characterizes slow-slow AVNRT. Neither the antegrade nor the retrograde fast pathway is necessary for this reentrant circuit and therefore the fast pathway may be absent. Characteristic of the slow-slow form of AVNRT is the presence of a lower common pathway.9

Fast-Slow

In fast-slow AVNRT, it is assumed that the fast AV nodal pathway is used as the antegrade limb and the slow AV nodal pathways as the retrograde limb. The ECG during tachycardia may show a P-R interval that is shorter than the R-P interval (long R-P tachycardia). The A-H interval is less than 180 ms, with P waves inverted in inferior leads. The H-A interval is longer than the A-H interval because of retrograde conduction over the slow AV nodal pathway. Similar to the slow-slow form, fast-slow AVNRT can be induced by atrial or ventricular stimulation, frequently during administration of isoproterenol. In addition, the presence of a lower common pathway results in an H-A interval during tachycardia that is shorter than that observed during ventricular stimulation. Earliest retrograde atrial activation is close to the CS ostium.

Left-Sided Variant

The left-sided variant occurs in up to 1.5% of patients undergoing ablation for AVNRT.^10,11 The activation pattern is usually that of slow-fast AVNRT. The diagnosis is confirmed by EP findings consistent with AVNRT but with successful slow pathway ablation from the LA after failure of RA ablation. The presence of a short H-A interval (≤ 15 ms) and the occurrence of antegrade double response to atrial pacing are sometimes noted in patients with this AVNRT variant. The A-H intervals and TCLs are shorter in the left-sided variant than in “right-sided” slow-fast AVNRT.

Ablation

Elimination of 1:1 conduction over the slow pathway is the target for ablation in all forms of AVNRT.^1,2,12 Once slow pathway conduction can be reproducibly demonstrated and the diagnosis of AVNRT is confirmed, the ablation catheter is positioned along the tricuspid annulus immediately anterior to the CS ostium. The RAO view is especially useful for positioning catheters because it displays Koch’s triangle en face. The angle of the left anterior oblique view should be adjusted so that the His catheter is perpendicular to the fluoroscopic plane. The initial target zone for slow pathway ablation is the isthmus of tissue between the tricuspid valve annulus and ostium of the CS. Figure 6.2 shows the locations of the mapping and ablation catheters. The targets for slow pathway ablation are given in Table 6.3. Three-dimensional (3D) electro-anatomic mapping systems such as CARTO (Biosense Webster, Diamond Bar, CA) or Ensite® (St. Jude, St. Paul, MN) can enable placement of diagnostic and ablation catheters and with little or even zero use of fluoroscopy and no exposure to the patient or staff to ionizing radiation. Figure 6.3 demonstrates an example of a typical 3D mapping approach to AVNRT.

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