Aurora Cardiovascular Services Case of the Month
ACS Editorial Board
Jasbir S. Sra, MD
Andrew Boyle, MD
Tanvir Bajwa, MD
David C. Kress, MD
Bijoy K. Khandheria, MD
A. Jamil Tajik, MD
Steven Port, MD
Masood Akhtar, MD
Microreentrant Atrial Tachycardia Five Years Following Left Atrial Ablation of Atrial Fibrillation
Daniel Hemsworth, M.D., Indrajit Choudhuri M.D., Jasbir Sra, M.D.
We report the case of a 68-year-old woman who presented with symptomatic persistent atrial tachycardia five years following left atrial ablation of atrial fibrillation (AF). Her initial ablation procedure in 2005 involved ostial pulmonary vein isolation and linear lesions (mitral isthmus, roof line, and right superior pulmonary vein to fossa ovalis) as part of a standard approach for elimination of persistent AF. Atrial tachycardias following ablation of AF are common and can develop during the ablation procedure itself or subsequently. Tachycardias that develop subsequent to the procedure tend to occur within the first few months and are generally macroreentrant in nature and related to gaps within ablation lines. Our patient, however, remained asymptomatic and off antiarrhythmic therapy for the intervening five years. To treat her symptomatic recurrent tachycardia, she was initiated on antiarrhythmic therapy with a Class III agent along with warfarin a few weeks prior to her repeat ablation. Despite antiarrhythmic therapy she continued to experience paroxysms of tachycardia and wished to discontinue the medication. Therefore, we pursued repeat electrophysiology study and ablation of her atrial tachycardia.
As her tachycardia did not develop until five years after her initial ablation procedure, it was unlikely the tachycardia was related to the previous procedure and the tachycardia-originating atrium was unknown. The clinical 12-lead ECG of her tachycardia suggested an upper left-atrial focus based on P-wave morphology. The P-waves were positive in the inferior leads, negative in lead AVL, and positive in lead V1 (see Figure 1). Electrophysiology study was performed and, as she presented in normal sinus rhythm, atrial tachycardia was induced with burst atrial pacing. This tachycardia was sustained with the same P-wave morphology as her clinical tachycardia. P-wave cycle length was 250 ms and intracardiac recordings revealed block in the mid-coronary sinus region as a result of the previous mitral isthmus ablation line. This location of block meant a perimitral tachycardia, which is commonly seen following AF ablation, was unlikely. Overdrive pacing from multiple right and left atrial sites prior to transseptal puncture revealed the tachycardia to be entrainable. With entrainment, the shortest post-pacing interval was 330 ms from the mid-coronary sinus, again implying a left-sided tachycardia.
Figure 1: Clinical tachycardia. P-waves with cycle length of 220 ms, positive in the inferior leads, negative in AVL and positive in lead V1, suggesting upper left-atrial focus.
Having localized the tachycardia to the left atrium, we introduced a quadripolar mapping/ablation catheter and a 64-pole multielectrode basket catheter into the left atrium using a double transseptal approach. We were then able to further localize the tachycardia to the left superior pulmonary vein ostium utilizing multiple imaging and mapping techniques. This localization was accomplished using three-dimensional (3D) electroanatomic mapping and CT-fluoroscopy fusion. In 3D electroanatomic mapping, three magnetic coils are placed under the patient enabling us to track our ablation catheter in space within the heart and, by correlating the timing of atrial depolarization with the endocardium in 3D space, create an activation map of the tachycardia (Figure 2). We correlated this area of earliest activation with an anatomic location by utilizing a CT-fluoro fusion technique that superimposes a live two-dimensional fluoroscopic image of the left atrium and our catheters over a previously acquired 3D CT reconstruction of the left atrium (Figure 3). Entrainability of the tachycardia, radial spread of activation on 3D mapping, and electrograms on the basket catheter spanning all of diastole made this tachycardia consistent with a microreentrant tachycardia.
Ablation of the tachycardia focus was performed using a 3.5-mm irrigated-tip ablation catheter. Using the basket recordings, we targeted the earliest electrograms within the left superior pulmonary vein. These early electrograms correlated with early activation on the 3D map, and ablation of these electrograms terminated the tachycardia.
Figure 2: Three-dimensional map of left atrium showing posterior view of left-atrial wall with orientation as noted and earliest activation (depicted in red) in the ostium of the left superior pulmonary vein, with radial spread of activation in all directions.
Figure 3: CT-fluoro fusion of left atrium in posteroanterior view with basket catheter in left superior pulmonary vein and ablation catheter in ostium of left superior pulmonary vein; red markers indicate location of ablation that terminated tachycardia.
Atrial arrhythmias are common following radiofrequency ablation of atrial fibrillation and seen in anywhere from 5% to > 50% of patients. Their occurrence is largely dependent on the extent of the original ablation procedure. Ablation of AF limited to pulmonary vein isolation carries a lower incidence of subsequent atrial tachycardias. However, in patients with persistent AF a more extensive ablation is often required, including formation of linear lesions and electrogram-guided lesions. A more extensive ablation increases the incidence of atrial tachycardias. Confirming complete isolation of the pulmonary veins and block across linear lesions at the time of the initial ablation decreases the incidence of subsequent atrial tachycardias (1), which usually manifest within a few months of the original ablation procedure. The mechanism of the tachycardias can be macroreeentrant, microreentrant or automatic. Macroreentrant tachycardias are the most common by far, accounting for roughly 75% in a large series described by Chae et al. (2). The remaining 25% of tachycardias are split relatively evenly between microreentrant (13%) and (12%) automatic. The fact that we were able to entrain the tachycardia by pacing at a cycle length 20-40 ms faster than the tachycardia, and that the basket catheter had electrograms spanning all of diastole, implied that it was reentrant. Localization was performed with 3D mapping, and the fact that the circuit was < 3 cm in diameter defined it as a microreentrant tachycardia. By targeting electrograms on the basket catheter, which correlated with earliest activity on the electroanatomic map, the tachycardia was terminated and rendered noninducible. Using these imaging and localization techniques and a well-planned approach to the repeat ablation, atrial tachycardias that occur following ablation of atrial fibrillation can be ablated with a high success rate, often obviating future medical therapies. Our patient’s antiarrhythmic and warfarin therapies were discontinued at the time of her ablation, and she has not had any recurrence of her arrhythmia now more than one month out.
- Morady F, Oral H, Chugh A. Diagnosis and ablation of atypical atrial tachycardia and flutter complicating atrial fibrillation ablation. Heart Rhythm 2009;6(8 Suppl):S29-32.
- Chae S, Oral H, Good E, et al. Atrial tachycardia after circumferential pulmonary vein ablation of atrial fibrillation: mechanistic insights, results of catheter ablation, and risk factors for recurrence. J Am Coll Cardiol 2007;50:1781-1787.
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