Left Atrial Posterior Wall Tachycardia Utilizing Alternating Exit Sites

Case Presentation

The patient is an 80-year-old man with a history of atrial fibrillation (AF), hypertension, hyperlipidemia, obstructive sleep apnea, and bradycardia status post pacemaker implant, pulmonary vein antral isolation (PVAI), and cavotricuspid isthmus ablation. Prior to his first ablation, the patient’s left atrial (LA) size was 50 mm by transthoracic echocardiogram in the parasternal long axis view.

Two years of paroxysmal AF preceded his first ablation, during which he developed progressive worsening of symptoms such as palpitations, shortness of breath, and fatigue. He did well postoperatively, but presented again 2 years later with more progressive symptoms. An electrocardiogram (ECG) revealed a ventricular paced rhythm with flutter waves of roughly 300 ms; this was most visible in leads II and V1 (Figure 1). P waves were positive in V1; thus, we suspected a LA origin for this arrhythmia. He was sent to our cardiac device clinic, where pacemaker interrogation revealed atrial tachycardia with a tachycardia cycle length (TCL) of approximately 295 ms on the atrial channel (Figure 2). His arrhythmia burden had escalated quickly, with 92% burden on presentation to the device clinic. Since he had undergone prior ablation with PVAI, it was expected that there would potentially be non-PV targets. Therefore, a more extensive ablation strategy beyond the PVs was expected and discussed with the patient.

He was brought to the electrophysiology lab for treatment of the arrhythmia. Using Coherent mapping with the Carto V7 system (Biosense Webster, Inc, a Johnson & Johnson company), a PentaRay mapping catheter (Biosense Webster) was delivered through an SL1 sheath (Abbott) via the right groin. A ThermoCool SmartTouch SF catheter (FJ Curve; Biosense Webster) was advanced through the Carto Vizigo bidirectional guiding sheath (Biosense Webster). In the left groin, a 10 French (Fr) intracardiac echocardiography (ICE) catheter was placed via a standard 10 Fr sheath. A decapolar coronary sinus (CS) reference catheter was also placed in the left groin via a standard 8 Fr sheath. No fluoroscopy was used in this case beyond collection of baseline CartoUnivu module (Biosense Webster) images.

ECG and decapolar CS activation were both indicative of left-sided etiology. A duodecapolar CS catheter to simultaneously examine right and left activation patterns would certainly have made this even more apparent. Transseptal puncture was performed with an SL1 sheath and Brockenbrough needle (Medtronic) using ICE. The needle was then exchanged for the SL1 wire, which was placed into the left superior PV. The ICE image of the wire across the septum was used to draw the transseptal location on the Carto map. The SL1 was pulled back into the right atrium and the ablation catheter was pushed across the transseptal site into the LA using Carto. The SL1 was then advanced across the septum into the LA, through which the PentaRay catheter was placed.

Voltage mapping revealed isolation of the PVs. Activation of the CS alternated consecutively between 290 and 330 ms, respectively, with slightly differing activation sequence morphologies (Figure 3). There were areas of scar adjacent to a diagonal tract of normal tissue on the posterior wall of the LA (Figure 4) by voltage mapping. Further, signal along the mid posterior wall of the LA was early and fractionated, denoted by a red pushpin (Figure 5). Early signal was noted along the posterior roof as well, although not quite as early as the mid-LA posterior wall. Activation, propagation mapping, and Coherent mapping (Figure 5, Video 1) revealed a LA tachycardia utilizing the posterior left atrial wall at the level slightly superior to the right PV carina posteriorly. The propagation map revealed early activation meeting late activation on the roof of the LA. Areas of slow conduction were noted near the posterior aspect of the left superior PV and posterior to the right inferior PV (Video 1).

Video 1. Activation, propagation, and Coherent maps are combined revealing tachycardia circuit running along the posterior wall with zones of slow conduction noted near the posterior aspect of the left superior pulmonary vein (PV) as well as posterior to the right inferior PV. Activation continues anteriorly after turning underneath both inferior veins. Activation continues superiorly on the anterior wall, ultimately turning posteriorly in viable tissue near the central aspect of the roof to complete the circuit.

The former PVAI lesion location was defined by voltage mapping. Our mapping system is configured with the VisiTag Surpoint Module (Biosense Webster) for greater ablation lesion precision. Ablation on the posterior wall was performed at 50 W for an automated annotation target value of 380. Esophageal temperature monitoring was used throughout this case, noted by the red catheter resting in the esophagus at the level of the superior PVs, where the PentaRay can also be seen resting in the left atrial appendage (LAA) (Figure 6). This linear lesion set was performed diagonally on the posterior wall from the posterior aspect near the former left superior PV isolation lesion set to the confluence of the right PV carina posteriorly. This progressively slowed the TCL, with ultimate tachycardia termination to normal sinus rhythm during completion of the diagonal lesion set (Figure 7, Video 1). The target value for all lesions was 10-15 g of contact force.

The alternating activation on the CS appeared to result from shifting exit sites on the posterior wall with resultant changes in CS activation morphology and cycle length. The voltage map helped to clarify and support the working diagnosis for the tachycardia circuit, which was further substantiated by the activation, propagation, and Coherent maps. The circuit moved from the roof along the posterior wall through the electrically active myocardium on the posterior wall. An apparent functional block within the posterior wall at the level of the carina of the PVs likely shifted, resulting in alternating exit sites with resultant dual TCLs and CS activation morphologies. Additionally, there was an apparent rotor near the posterior aspect of the left superior PV (Video 1). The activation continued from the posterior wall, turning under the left and right PVs heading anteriorly, respectively. The activation course was lost as it ran along the epicardium both near the mitral isthmus and anterior to the right PVs. Subsequent activation continued superiorly on the LA anterior wall as it converged at the roof. Entrainment was considered but not performed due to concern of altering a potentially tenuous, fluctuating tachycardia circuit. During the course of the ablation, the TCL slowed; at this point, our clinical account specialist switched from activation mapping to voltage mapping to locate the putative ablation endpoint. As the ablation catheter neared the interface from healthy tissue to electrically inert tissue, the tachycardia terminated to sinus rhythm. Following venous access site closure with the Vascade closure device (Cardiva Medical), the patient was discharged the same day and has been arrhythmia free for 6 months.

Discussion

This ablation strategy best addresses what was seen with Coherent, activation, and propagation maps, yet also follows where electrically active tissue resided reflected by the voltage map, which is our usual practice when deciding on the best ablative course of action. To improve contact and stability, ventilator settings are adjusted during ablation with a respiratory rate of 30 bpm, tidal volume of 200 cc, and I:E ratio of 1:4, which minimizes cardiac motion related to respiratory variation.

We feel this significantly improves the quality and efficiency of ablation lesions. This is further refined with the combined use of Vizigo, Surpoint, and the mapping lesion distance tool. We found the dual TCLs and morphologies in this case to be fascinating. A retrospective and alternative possible diagnosis of the alternating CS activations and morphologies held that the shorter TCL represented the apparent rotor posterior to the left superior PV. In this postulated scenario, the longer TCL reflects the longer circuit running from the posterior wall turning anterior under both inferior PVs and continuing superiorly to merge at the roof to complete the circuit. In fact, as ablation continues, the TCL increases with activation shifting and becoming one morphology, which could represent termination of the rotor with progressive delay of the longer circuit that used both the posterior and anterior walls of the LA (Figure 8, Video 1).

Acknowledgements. A special thanks to Biosense Webster Senior Clinical Account Specialist Kurt Shults for cardiac mapping and media collection.

Disclosures: The author has completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Smith has no conflicts of interest to report regarding the content herein.