Retrograde fast pathway ablation with the EnSite NavX mapping system for slow–fast atrioventricular node reentrant tachycardia and a prolonged PR interval during sinus rhythm

Summary

An 84-year-old male had experienced palpitations. He was transported to our hospital for treatment of palpitations. A 12-lead electrocardiogram (ECG) showed regular tachycardia with a wide QRS complex of 153 bpm, and the P wave was not clear. The ECG after the tachycardia stopped showed a sinus rhythm, and there was a prolonged PR interval of 312 ms and complete right bundle branch block. We recorded a prolonged AH interval (235 ms) in electrophysiology study (EPS). As for the St-A interval (185 ms) by consecutive pacing from the right ventricular apex, it was short in comparison with the anterograde conduction. As a result of detailed EPS, we diagnosed the tachycardia as slow–fast atrioventricular nodal reentrant tachycardia. The anterograde conduction depended on the slow pathway (SP), and the fast pathway (FP) was considered to have only retrograde conduction. It was thought that a complete atrioventricular block been caused by the SP ablation. Therefore we carried out FP ablation with three-dimensional computed tomography and the EnSite NavX mapping system (St. Jude Medical, St Paul, MN, USA), which was superior in space resolution power, and were able to effect a radical cure without complications.

Introduction

There are two circuits, called the slow pathway (SP) and the fast pathway (FP), in the electric conducting pathway to the compact atrioventricular node [1], [2]. When premature atrial contraction is generated during the refractory period of the FP, anterograde conducts SP and FP oppositely, and it is thought that it includes perinodal atrial tissue in a circuit and causes atrioventricular nodal reentrant tachycardia (AVNRT) [3]. Radiofrequency catheter ablation is widely performed as part of a radical cure at present, and radical cure of tachycardia is also possible by SP ablation [3], [4], [5].

In addition, during recent years, three-dimensional (3-D) mapping has been combined with three-dimensional computed tomography (3-DCT) [6]. It is now possible to display detailed anatomy that was hard to understand when only using fluoroscopy, and this is an effective means for elucidation of arrhythmia and catheter ablation.

We treated a case of slow–fast AVNRT in which the FP had only retrograde conduction. It was thought that SP ablation was very likely to have led to a complete atrioventricular block [3], [4], [5]. A report of a study using only fluoroscopy has appeared, but there has not yet been a report on using 3-DCT with 3-D mapping together. Therefore we carried out FP ablation with 3-DCT and the EnSite NavX mapping system (St. Jude Medical, St Paul, MN, USA), which was superior in space resolution power, and were able to effect a radical cure without complications [7].

Case report

The case was an 84-year-old male. Anterior-septal wall myocardial infarction had been caused from anamnesis at the age of 69, and the patient had had coronary angioplasty to the left anterior descending artery. There were no especially significant hereditary factors to be considered. He had noticed palpitations once every 2 or 3 months for around 6 years, but the symptoms were improved by rest. One day he noticed palpitations while walking home from work and was not able to stand. A passer-by gave first aid, and the subject was taken to our hospital. A 12-lead electrocardiogram (ECG) during transportation showed a regular tachycardia of wide QRS complex in 153 bpm, and the P wave ahead of the QRS complex was not clear. The P wave of the QRS complex front and back was also not clear, probably because there was a complete right bundle branch block (CRBBB) (Fig. 1A). The tachycardia was stopped by injection of a dose of adenosine triphosphate (10 mg). The ECG after the tachycardia stopped showed a sinus rhythm, and there was a prolonged PR interval of 312 ms and CRBBB (Fig. 1B). A prolonged PR interval ensued. From the above, it was supposed that the anterograde conduction of the atrioventricular node depended on SP, or that the His–Purkinje system was affected. Because the patient hoped for a radical cure, we did an EPS and carried out catheter ablation on the fourth day after admission.

Figure 1.

The electrocardiogram (ECG) of the tachycardia and sinus rhythm. (A) The ECG showed a regular tachycardia of wide QRS complex in 153 bpm, and the P wave did not become clear. (B) The ECG showed a prolonged PR interval (312 ms) and complete right bundle branch block for sinus rhythm.

We inserted an electrode catheter to the right atrium (RA), coronary sinus (CS), His bundle, and right ventricle (RV). The AH interval was prolonged, with AA interval of 712 ms, AH interval of 235 ms, HV interval of 46 ms for sinus rhythm at the start (Fig. 2A). Although there was CRBBB, the PR interval prolongation by the obstacle of His bunch or His–Purkinje system was negative. As for the V-A interval of 135 ms by RV apex pacing, it was clearly short in comparison with the anterograde conduction (Fig. 2B). It was thought that the conducting pathway retrograde and the anterograde conducting pathway were different circuits. Atrioventricular conduction was 1 to 1 conduction to 130 ppm by consecutive pacing from high RA. The AH interval showed a conduction delay in response to an increase in the rate by extra pacing from the RA and the AH interval did not show jump (Fig. 2G). The effective refractory period (ERP) of the atrioventricular node was 250 ms. Ventriculoatrial (VA) conduction was 1 to 1 conduction to 120 ppm, and the ERP of VA conduction was 320 ms. The VA interval showed a conduction delay in response to an increase in the rate by extra pacing from the RV apex (Fig. 2G). Because the St-A interval during para-Hisian pacing resulting in narrow QRS complex was shorter than that during pacing resulting in wide QRS complex, the presence of the accessory pathway was excluded (Fig. 2C) [8]. We had no evidence of dual pathway physiology or anterograde FP conduction either at baseline or during isoproterenol infusion.

Figure 2.

Surface electrocardiogram and intra-cardiac electrocardiogram. (A) Control electrophysiology study: only AH interval prolonged it in AA interval of 712 ms, AH interval of 235 ms, HV interval of 46 ms for sinus rhythm. (B) During the RV pacing: as for St-A interval (185 ms) by RV apex pacing, it was clearly short in comparison with the anterograde conduction. (C) Para-Hisian pacing: St-A interval extended it by para-Hisian pacing in the refractory period of His brunch. (D) Tachycardia: the cycle length of the tachycardia is 432 ms, and VA interval is 54 ms in His catheter. (E) Reset: a ventricular stimulus delivered during His bundle refractoriness fails to advance the tachycardia. (F) Entrainment by RV apex pacing: it extended the post pacing interval and the difference of the cycle length with 134 ms in entrainment by RV apex pacing. (G) A conduction curve of AH interval and VA interval: triangle AH interval. Circle VA interval.

The tachycardia was caused easily by extra pacing from RA. The cycle length of the tachycardia was 432 ms, and VA interval was 54 ms in the His catheter [9]. The earliest atrial deflection was detected in a His catheter. The sequence of atrial deflection of tachycardia was the same as that of pacing from the RV apex (Fig. 2D). A ventricular stimulus delivered during His bundle refractoriness failed to advance the tachycardia (Fig. 2E) [10]. It extended the post pacing interval and the difference of the cycle length to 134 ms in entrainment from RV apex pacing (Fig. 2F) [11]. We diagnosed slow–fast AVNRT from the above. The anterograde conduction depended on SP, and the FP was regarded as showing only retrograde conduction. It was thought very likely that a complete atrioventricular block had been caused by the SP ablation. Therefore we attempted ablation of the FP.

We judged that it was very likely that the FP ablation only with fluoroscopy had caused a complete atrioventricular block. Therefore we used the EnSite NavX mapping system for 3-D mapping and tried ablation.

We recorded the His bundle deflection and slow pathway potential by contact mapping with an ablation catheter (Ablaze Fantasista MMcurve 4 mm-tipped/Japan Lifeline Co, Ltd., Tokyo, Japan) during sinus rhythm and we recorded atrial deflection under slow–fast AVNRT. We recognized the His bundle deflection in a range 32 mm in length, and 14 mm in width. The earliest atrial deflection at the time of slow–fast AVNRT in this case recorded it in the 15 mm (recognized at the position of 6 mm posterior to HB, 8 mm superior to HB) stern side from the atrium edge where the His bundle deflection was recorded. We considered that the earliest atrial deflection was FP (Fig. 3) [12]. The anterograde conduction depended on SP, but the earliest atrial deflection was different from the place of SP. Thus, we considered that we could avoid atrioventricular block even if we did ablation for retrograde conduction FP. We explained that we would implant a pacemaker if atrioventricular block occurred to the patient and decided to do ablation after having obtained his consent. We ablated the part during sinus rhythm. The current was initially applied at a power output of 10 W and after we confirmed that there was no prolongation of the AH interval, the power output was increased by 5 W every 10–15 s to a maximum output of 25 W. After ablation, the AH interval (250 ms) and HV interval (51 ms) had not changed (Fig. 4A). Atrioventricular conduction was 1 to 1 conduction to 120 ppm by consecutive pacing from high RA, and the ERP of atrioventricular node was 230 ms. The VA conduction disappeared with intravenous administration of isoproterenol (0.02 μg/kg/min) (Fig. 4B).

Figure 3.

(A) Activation map during slow–fast atrioventricular nodal reentrant tachycardia (AVNRT) in the Ensite NavX image. Inner view of right anterior oblique. Earliest atrial deflection at the time of slow–fast AVNRT in this case accepted it in the 12 mm (recognized it at the position of 6 mm posterior to HB/8 mm superior to HB) stern side from the atrium edge where His bundle deflection was recorded. (B) The position of the ablation catheter at the earliest activation site in the endocardium (upper: right anterior oblique; lower: left anterior oblique). (C) Surface electrocardiogram and intra-cardiac electrocardiogram of ablation site.

Figure 4.

After ablation. (A) AH interval (250 ms) and HV interval (51 ms) without a change. (B) Ventriculoatrial conduction disappeared.

After ablation, the pacing from RV showed a total VA dissociation, and it was thought that we had succeeded in a solution of the FP. The obstacle was not caused in anterograde conduction, and there was no atrioventricular block or other complications. One year has passed, but there are no symptoms that suggest AVNRT, nor evidence of second or third degree atrioventricular block.

Discussion

We were faced with a case in which anterograde conduction depended on SP, but the FP had only retrograde conduction, and slow–fast AVNRT occurred. In the case of slow–fast AVNRT, SP ablation is currently performed by an anatomical method or potential index [3], [5]. However, some patients with AVNRT have a prolonged PR interval in the surface ECG. This leads us to suppose that these patients have a weak FP or do not have anterograde FP conduction. It was thought very likely that a complete atrioventricular block would occur if the SP was ablated in these cases. Therefore we ablated the FP. If FP ablation only by fluoroscopy were used it was thought very likely that a complete atrioventricular block would happen. Thus, to reduce risks, a 3-DCT system was used and the index was increased to make spatial position relations clear with the EnSite NavX mapping system, which was superior in space resolution power [6], [13]. We were able to effect a radical cure without complications.

The subject of where the earliest atrial deflection in slow–fast AVNRT can be recorded is controversial. A report of a study using only fluoroscopy has appeared, but as yet, no report using 3-D mapping together with 3-DCT [12] has been produced. This result may put an end to disputes on this matter. However, the results are appropriate only for the small patient population studied, and cannot be generalized to all patients. This problem could be resolved in future by examining similar cases in detail.

In conclusion, for slow–fast AVNRT in which FP has only retrograde conduction, the detailed mechanism of the tachycardia could be clarified by using the EnSite NavX mapping system incorporating not only fluoroscopy but also 3-DCT, and a radical cure could be achieved without complications by ablating the FP.