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Cardiology Research

Case Report

Volume 10, Number 1, February 2019, pages 48-53

A Retrograde Transaortic/Transmitral Approach for Radiofrequency Ablation of Adenosine-Sensitive Atrial Tachycardia Arising Near the Apex of Koch’s Triangle: A Case Study Approach and Review of the Literature

Atrial tachycardias (ATs) are relatively uncommon and most of them originate from the right atrium, particularly arising along the crista terminalis [1-6]. The mechanisms of AT include reentry or may be focal due to abnormal automaticity or triggered activity [7, 8]. Reports describing a distinct entity of paroxysmal AT originating in the atrioventricular (AV) junction which mimics common or uncommon AV nodal reentrant tachycardia and can be ablated from the right atrial septum have been published [9, 10]. We report a case of this tachycardia in which successful radiofrequency (RF) ablation was performed from the left atrial septum by using a retrograde transaortic/transmitral approach.

A 63-year-old woman with no evidence of structural heart disease suffered from recurrent supraventricular long RP tachycardia nonresponsive to beta-blockers. A 12-lead electrocardiogram (ECG) showed a narrow QRS tachycardia at a rate of 130 - 150 beats per minute (bpm), with shallow inverted P waves in the inferior leads and an RP/PR ratio > 1.

An electrophysiological study was performed using four multipolar catheters with 10 mm interelectrode spacing (Daig, St. Jude Medical, St. Paul, MN, USA). Quadripolar catheters were used for stimulation and recording from the high right atrium and the right ventricular apex. Two hexapolar catheters were positioned within the coronary sinus for left atrial activity recording and across the tricuspid valve for His-bundle (distal pair) and low right atrial (proximal pair) activity recording. A steerable quadripolar 7-French catheter with a 4 mm tip electrode (Marinr, Medtronic, Minneapolis, MN, USA) was used for mapping the right atrium, the noncoronary sinus of Valsalva and the left atrium, and temperature-guided RF ablation. Mapping of the left atrium was performed by using a novel retrograde transaortic/transmitral approach. Briefly, the Marinr MC, a steerable multicurve catheter was placed via the femoral artery and advanced into the left ventricle with the catheter tip positioned at the posterolateral mitral annulus from the left ventricular aspect. Then, with a minimum curve (40 mm) under fluoroscopy and intracardiac recording, the tip was gently deflected (the Tip Deflection Control) and counterclockwise rotated (the Lateral Deflection Control) under careful increasing of the deflected curve (the Curve Radius Control) until the catheter tip was advanced into the left atrium verified by fluoroscopy along with recording a high-amplitude atrial activity. Further steering of the catheter tip using all the three Controls enabled mapping and ablation in the left atrium.

The electrophysiological study performed during sinus rhythm showed continuous anterograde AV nodal and no ventriculoatrial (VA) conduction. Tachycardia could be induced and terminated by atrial pacing and atrial extrastimulation (Fig. 1a). Tachycardia induction was unrelated to a critical AH delay and VA dissociation could be demonstrated by ventricular stimulation during tachycardia. The earliest atrial activation was recorded in the His-bundle region. Atrial extrastimulation performed during tachycardia showed an inverse relationship between the reset return cycle and atrial extrastimulus prematurity. Intravenous administration of 6 mg adenosine reproducibly terminated the tachycardia preceded by prolongation of the tachycardia cycle length without developing AV nodal block (Fig. 1b).

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Figure 1. Findings from the electrophysiological study. (a) Intracardiac recordings showing tachycardia induction with an atrial extrastimulus at a prematurity (S1S2) of 390 ms coupled with a drive cycle length (S1S1) of 462 ms. Paper speed = 100 mm/s. (b) Tachycardia termination after intravenous bolus of 6 mg adenosine. Paper speed = 75 mm/s. A1, A2, and Ae: atrial electrograms; CSP, CSM, and CSD: proximal, middle, and distal coronary sinus, respectively; HRA: high right atrium; HBE: His-bundle electrogram; LRA: low right atrium; RV: right ventricular apex.

Fractionated RF ablation was unsuccessful at the right atrial mid-septum near the apex of Koch’s triangle, where a His-bundle was recorded, despite recording an early local atrial activity of 48 ms before the P wave. Mapping the noncoronary sinus of Valsalva found no earlier atrial activity. By using a retrograde transaortic/transmitral approach, the ablation catheter was positioned in the low left atrial septum opposite the His-bundle catheter (Fig. 2a, b). Endocardial mapping showed the earliest atrial activity of 52 ms before the P wave without a recordable His-bundle potential (Fig. 2c) along with a perfect pace map (Fig. 2d, e). Single RF application at this site resulted in prompt tachycardia termination (Fig. 3) followed by infrequent atrial ectopic beats. After ablation, the tachycardia was no longer inducible and no damage to the AV node was observed.

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Figure 2. Findings from the retrograde transaortic/transmitral approach. (a) Right anterior oblique and (b) left anterior oblique radiographs of the RF ablation catheter positioned at the successful ablation site of left atrial septum. White arrows indicate the tip of a steerable catheter positioned in the right atrial mid-septum (RMS). (c) Bipolar electrogram from the RF catheter during tachycardia. The local atrial electrogram precedes the P wave by 52 ms without a recordable His-bundle potential. (d) Twelve-lead ECG during tachycardia. (e) Perfect pace map obtained from the successful ablation site. The other abbreviations are shown in Figure 1.

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Figure 3. RF ablation of the tachycardia. Delivery of RF energy promptly terminates the tachycardia.

Reports on AT arising from near the apex of Koch’s triangle have been published. The incidence of this tachycardia varies between 0 to 37% among patients with ATs [9-11]. Factors as patient selection and the fact that this tachycardia mimics common or uncommon AV nodal reentrant tachycardia may be responsible for the varying incidence. It has been speculated that RF modification of the AV node might cure this tachycardia [10]. However, it remained inducible despite complete AV nodal block caused by ablation and its elimination did not influence dual AV nodal physiology [9].

In the present case, the tachycardia could be terminated by intravenous adenosine. The electrophysiologic findings in our patient were consistent with the diagnosis of adenosine-sensitive AT arising from near the apex of Koch’s triangle [9]. The mechanism of this tachycardia has been attributed to reentry in the transitional area of the AV node or triggered activity [9, 12-15]. Previous studies have shown successful ablation of this tachycardia from the right atrial septum near the His bundle or AV node without disturbing AV nodal conduction [9-11]. It has been shown that transseptal mapping and ablation from the left side of the interatrial septum were required for some focal ATs originating from the vicinity of the AV node [16, 17]. However, the possibility that those ATs are adenosine-sensitive was not studied. As previously reported, some of these ATs can be eliminated by ablation from the noncoronary aortic cusp [18]. RF energy delivery through the aortic sinus of Valsalva is associated with several potential complications including embolic events and the risk of injuring the coronary arteries and perforating the sinus of Valsalva. However, several subsequent studies reported that these ATs can be ablated successfully and complication-free from the noncoronary aortic cusp [17, 19-25]. Although ablated from the noncoronary aortic cusp, both the electrophysiologic characteristics and the sensitivity to adenosine were also suggestive of triggered activity or micro-reentry as a mechanism responsible for this focal AT [19]. These ATs eliminated from the right atrial anterior septum or the noncoronary cusp are believed to be located in the true atrial septum [22]. It has been reported that the minority of ATs conventionally with the earliest atrial activation in the His-bundle region and negative P waves in leads I and aVL can be located and ablated from the left coronary cusp via a retrograde aortic approach or in the aortic mitral junction via a transseptal approach [17, 26-30]. Mapping the noncoronary sinus of Valsalva in this case found no early activity. Our report is the first one we are aware of demonstrating successful RF ablation from the left atrial septum by using a special technique for the retrograde transaortic/transmitral approach. Our transaortic/transmitral approach seems to be a continuation of an ablation strategy proposed by Wang et al [22], consisting of a right atrial trial, and if needed, followed by a retrograde aortic approach. In case of failure of this strategy in AT with negative P waves in leads I and aVL, our approach may enable left atrial mapping and ablation in the aortic mitral junction, as successfully done in our another case (unpublished data). In one case reported by Joung et al [31], no early atrial activation was found in the left atrium using a retrograde transaortic approach and successful AT ablation was performed from the noncoronary aortic cusp. However, in their case, radiographs showed that the left atrial catheter was placed deep in the left atrium far away from the left basal anterior septum. The fact that AV junctional cells histologically similar to atrial cells but resembling nodal cells in their cellular electrophysiology and response to adenosine have been found around both AV annuli [27, 32-35] is in support of the possibility that this adenosine-sensitive tachycardia can be located and ablated on the left side of the interatrial septum.

For ATs that are inducible and terminable with stimulation, discrimination between intra-atrial reentry and triggered activity may be difficult. Atrial reentry tachycardia was usually characterized by an inverse resetting response pattern, whereas triggered AT was designed for those with a direct resetting response [9, 36, 37]. In eight of nine patients with triggered AT with demonstrable delayed afterdepolarization in monophasic action potential, mixed and inverse types of resetting response pattern were found in six and two patients, respectively [36]. Similar findings were also reported by others [38, 39]. Thus, inverse resetting response pattern does not appear to be specific for reentry. Therefore, tachycardia termination by intravenous low-dose adenosine was rather suggestive of triggered activity as the mechanism in our case [40]. However, the possibility that the mechanism of this focal tachycardia is micro-reentry [9, 12] or reentry in a small circuit due to markedly nonuniform anisotropic conduction properties [41] cannot be excluded. As reported in the latter study, nonuniform anisotropic cellular coupling, which is associated with underlying microfibrosis, makes it possible for reentry to occur in small areas (< 10 - 15 mm²).

In conclusion, our findings demonstrate the feasibility of retrograde left atrial ablation of adenosine-sensitive tachycardia arising from near the apex of Koch’s triangle. We believe that patients with unsuccessful right-sided ablation of this tachycardia may require a left atrial approach to eliminate it.

Conflict of Interest

The authors declare that there is no conflict of interest or financial relationship regarding the publication of this paper.

Consent

The patient gave her informed consent prior to inclusion in the study and the ethics committee approval was obtained.

Abbreviations

AT: atrial tachycardia; AV: atrioventricular; RF: radiofrequency; ECG: electrocardiogram; bpm: beats per minute; VA: ventriculoatrial

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