Catheter Ablation of Atrial Tachycardia Originating From the Posterior Wall of the Left Atrium Following Prior Atrial Fibrillation Ablation: A Case Report

ABSTRACT

This case report describes a 56‐year‐old male with recurrent symptomatic atrial tachycardia (AT) following prior extensive atrial fibrillation ablation, including posterior wall isolation. Surface ECG suggested a possible pulmonary vein origin, but high‐density 3D electroanatomic mapping precisely localized the focus to the left atrial posterior wall. Radiofrequency ablation at the earliest activation site terminated the tachycardia promptly. The patient remained symptom‐free during a 3‐month follow‐up. This case highlights the importance of detailed mapping in localizing rare AT origins after prior ablation, the challenges of ECG interpretation in altered substrates, and the feasibility of safe and effective ablation in the posterior wall region with controlled energy delivery.

Key Clinical Message.

Atrial tachycardia originating from the left atrial posterior wall is rare and may occur despite prior isolation. Successful ablation requires high‐density 3D mapping for precise localization and careful parameter control near the esophagus to ensure safety and efficacy.

1. Introduction

Focal atrial tachycardia (AT) is a subtype of supraventricular arrhythmia originating from discrete atrial foci. Common sites include the crista terminalis, tricuspid annulus, pulmonary vein orifices, and mitral annulus. The complex anatomy of these regions poses challenges for precise electrophysiological mapping and stable catheter contact during ablation, potentially leading to lower procedural success rates compared to other supraventricular tachycardias. Of note, AT usually occurs in areas of anisotropic substrate, yet the distribution of myocardium within the left posterior wall is relatively homogeneous, which is why AT originating specifically from the posterior wall of the left atrium is exceedingly rare, representing < 5% of focal ATs. Due to the altered substrate by prior ablation, obscured localization by prior lesions, and increased risk of esophagus injury by being close to the esophagus, the ablation of AT from the left atrial posterior wall is particularly challenging in patients with prior AF ablation. The mechanism of such ATs in this setting remains poorly characterized, representing a knowledge gap in post‐ablation arrhythmia management. This report presents a case of successful RFCA for AT originating from the left atrial posterior wall after extensive prior AF ablation, highlighting the procedural strategy and clinical outcome.

2. Case History

A 56‐year‐old Han Chinese male was admitted with complaints of intermittent palpitations for 14 years, which had exacerbated over the previous month. The palpitations were accompanied by chest tightness and shortness of breath. His medical history was significant for a percutaneous coronary intervention (PCI) performed four months prior and a radiofrequency ablation for persistent atrial fibrillation two months prior, which included bilateral pulmonary vein isolation, posterior wall isolation, and cavotricuspid isthmus block. The patient experienced initial symptom relief for approximately one month post‐AF ablation before the recurrence of sustained palpitations, suggesting a temporal link between the prior ablation and the development of this AT. A 24‐h Holter monitor revealed paroxysmal atrial tachycardia accounting for 96.21% of the recording duration. The patient provided written informed consent for the publication of his clinical details.

3. Differential Diagnosis, Investigations, and Treatment

The 12‐lead surface ECG during AT (Figure 1) showed a positive P wave in lead V1, a biphasic (+/−) P wave in lead aVL, and upright P waves in leads II, III, and aVF. These features initially suggested a possible origin near the right upper pulmonary vein based on conventional ECG algorithms. However, in the setting of left atrial enlargement and prior ablation, ECG specificity is reduced, as these factors can alter P‐wave morphology. Echocardiography revealed left atrial enlargement (47 mm) and a mildly reduced left ventricular ejection fraction (LVEF) of 51.75%.

FIGURE 1.

Twelve‐lead electrocardiogram during atrial tachycardia. Note the positive P wave in lead V1, biphasic (+/−) P wave in lead aVL, and upright P waves in leads II, III, and aVF.

Due to the high burden of AT and symptomatic deterioration, a repeat catheter ablation was recommended. Written informed consent was obtained from the patient according to journal guidelines.

During the procedure, a decapolar catheter was placed in the coronary sinus (CS) and a bipolar electrode in the right ventricle. Spontaneous narrow QRS tachycardia (cycle length 195 ms) with an RP’ > P'R pattern was observed and remained stable throughout mapping. A V‐A‐A‐V response following overdrive ventricular pacing supported a left atrial origin. A transseptal puncture was performed. High‐density activation mapping of the left atrium was conducted using the ENSITE system with an Advisor HD Grid mapping catheter. Approximately 1200 points were collected throughout the left atrium, with dense sampling over the posterior wall. Mapping revealed the earliest atrial electrogram on the posterior wall of the left atrium, rather than the pulmonary veins (Figure 2). The local electrogram at this site preceded the surface P wave by 124 ms (Figure 3). The electrogram at the successful site was discrete and early, without significant fractionation. Radiofrequency ablation was delivered at this site (max power 40 W, temperature limit 43°C, lesion duration limited to 20–30 s per application), which terminated the tachycardia within 11 s. Post‐ablation, no tachycardia was inducible, and the procedure was concluded successfully. No esophageal temperature monitoring or other protective strategies were used. Because the aim of the ablation of AT is the termination of this arrhythmia, and usually the focus of the ablation target tissue is superficial without the need for transmural ablation, so provided that the power, temperature, and duration of the ablation are appropriately controlled, the risk for esophageal injury is low. The other reason is that esophageal temperature monitoring or other protective strategies are not routinely and widely used in China.

FIGURE 2.

Electroanatomic Map and Intracardiac Electrograms. (A) Activation map of the left atrium (posterior view) showing the earliest activation site (red) on the posterior wall. (B) Intracardiac recordings demonstrating the local atrial electrogram at the ablation site preceding the surface P wave by 124 ms.

FIGURE 3.

Intracardiac electrograms demonstrating the local atrial electrogram at the ablation site (arrow) preceding the onset of the surface P wave by 124 ms.

4. Conclusion and Results

The patient's symptoms resolved completely after the procedure. Immediate post‐procedural ECG confirmed sinus rhythm. During a 3‐month follow‐up period, there was no recurrence of tachycardia by ambulatory rhythm monitoring, and the patient reported sustained symptomatic improvement. This case confirms that AT originating from the left atrial posterior wall presents with characteristic but not entirely specific ECG patterns and can be successfully treated with RFCA guided by high‐density mapping. The 3‐month follow‐up, while demonstrating acute success, is a limitation in a patient with such a complex atrial substrate, and longer‐term monitoring is warranted to assess durability.

5. Discussion

Focal atrial tachycardia (AT) mechanisms include enhanced automaticity, triggered activity, or micro‐reentry. Left atrial ATs most commonly originate from the pulmonary veins, but other sites like the mitral annulus, left atrial appendage, and posterior wall are also recognized [1]. This case is instructive due to the origin at the posterior wall, a relatively rare site, and its occurrence after extensive prior ablation for atrial fibrillation. Given the focal origin on high‐density mapping and abrupt termination with ablation, the most likely electrophysiological mechanism in this case is enhanced automaticity. This focus may have arisen from a surviving cluster of cardiomyocytes within or at the border of the prior posterior wall isolation area, possibly facilitated by the altered electrophysiological milieu post‐ablation. The surface ECG remains a valuable initial tool for localizing AT. A positive P wave in V1 is a strong predictor of left atrial origin [2]. However, as demonstrated here, distinguishing between origins in the pulmonary veins and the posterior wall proper can be challenging based on ECG alone. Factors such as atrial enlargement, prior ablation lesions, and individual anatomical variations can alter P‐wave morphology, limiting the specificity of ECG criteria [3]. Therefore, 3D electroanatomic mapping is essential for precise localization, as it was in this case where the earliest site was definitively mapped to the posterior wall.

Ablation in the left atrial posterior wall carries specific risks, most notably the potential for esophageal injury due to its close anatomical proximity. This necessitates precise, controlled ablation with careful attention to power and duration to minimize collateral damage while ensuring efficacy. The strategy of using a high‐density mapping catheter to pinpoint the earliest activation site allows for targeted ablation, potentially reducing the extent of tissue damage, lesion burden, and procedural risk. In this patient, the prior history of atrial fibrillation and extensive ablation may have created a substrate for this focal AT. The successful ablation at the posterior wall site highlights that RFCA is a viable option for managing such complex, post‐ablation arrhythmias. This case also underscores that posterior wall isolation does not guarantee protection against all posterior wall arrhythmias. Furthermore, the management of such arrhythmias may have implications for understanding complex arrhythmia substrates in conditions like cardiac syndrome X [4] and highlights the importance of precise mapping, akin to the targeted approach used in neuromuscular electrical stimulation for post‐operative recovery [5].

Author Contributions

Ying Gong: conceptualization, methodology, writing – original draft. Zhen Yang: supervision, writing – review and editing. Ali Ma: data curation, software, validation.

Funding

The authors have nothing to report.

Ethics Statement

This case report was conducted in accordance with the ethical principles outlined in the Declaration of Helsinki and adhered to the guidelines set forth by the Clinical Case Reports Institutional Review Board (IRB). The authors declare no conflicts of interest related to the content of this case report. This report was prepared solely for educational and scientific purposes, to contribute to the medical literature and enhance clinical knowledge.

Conflicts of Interest

The authors declare no conflicts of interest.

Data Availability Statement

Data sharing not applicable to this article as no datasets were generated or analysed during the current study.