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Abstract & Commentary
Synopsis: Focal left atrial tachycardias are an important complication after pulmonary vein isolation.
Source: Gerstenfeld EP, et al. Circulation. 2004;110: 1351-1357.
Pulmonary vein isolation has become increasingly popular as a treatment for patients with both paroxysmal and persistent atrial fibrillation. In this paper, Gerstenfield and colleagues address 1 of the more common complications associated with atrial fibrillation ablations.
Gerstenfield et al reviewed data from 341 patients who underwent pulmonary vein isolation for paroxysmal (86%) or persistent (14%) atrial fibrillation. The techniques used by Gerstenfield et al at the initial procedure involved placement of a circular mapping catheter in the pulmonary veins, and a search for atrial fibrillation within the veins. If arrhythmogenic atrial activity was located in 1 of the pulmonary veins, circumferential lesions were placed around the veins to isolate them from the rest of the atrium. No attempt was made to isolate all veins if they didn’t manifest arrhythmogenic potentials, nor were left atrial linear lesions used. A total of 955 arrhythmogenic pulmonary veins were isolated in the 341 patients. In the entire group, 68 patients had recurrent atrial fibrillation after ablation, and 10 of the 68 also developed a persistent left atrial tachycardia. These 10 patients returned for electrophysiologic study with mapping and attempt at ablation 5.7 ± 2.8 months after the initial procedure.
Characteristic ECG patterns were seen in the 10 patients with left atrial tachycardias. The ECG revealed regular activation that was positive in the inferior leads in 8 out of 10 patients. Atrial depolarization was predominantly positive in V1 and remained positive across the precordium in 8 of 10 patients. The surface ECG features of atrial activity could be used to diagnose the pulmonary vein that was the site of origin. For arrhythmias from the left superior pulmonary vein, atrial activity was flat in lead I, of lower amplitude in lead II than in lead III, negative in aVL, and M-shaped in V1. For right superior pulmonary vein origin tachycardias, the P wave was positive in lead I, was larger in lead II than in lead III, flat to biphasic in lead aVL, and had a late peaking positive wave in V1.
The site of origin was identified using electroanatomic mapping. A focal origin with a concentric spread of activation was noted in 8 patients. Of these, 6 of the tachycardias originated from partially reconnected pulmonary vein ostia. One patient exhibited a tachycardia that rapidly degenerated to atrial fibrillation rapidly, and therefore, could not be characterized. One patient had a macroreentrant tachycardia that traveled around the left upper and left lower pulmonary vein ostia. In the 8 cases of focal tachycardias, the tachycardia was localized and terminated with radiofrequency energy applied at the site of earliest activation. In the patient with a focal tachycardia that rapidly degenerated to atrial fibrillation, and in the patient with the macroreentrant tachycardia, linear lesions were placed guided by electroanatomic mapping, as well as repeat isolation of the pulmonary veins. After 6.7 ± 2.3 months of follow-up, 9 of the 10 patients remained arrhythmia free. Four of these patients, however, remained on antiarrhythmic therapy.
Gerstenfield et al conclude that focal left atrial tachycardias are an important complication after pulmonary vein isolation. In this series, focal ablation of the tachycardia at the earliest site of activation, reisolation of reconnected pulmonary veins, and antiarrhythmic drugs provided adequate therapy.
Comments by John P. DiMarco, MD, PhD
A number of different techniques are currently used for catheter ablation of atrial fibrillation. The technique used in this paper is similar to the approach originally developed by Haissaguerre and colleagues (Circulation. 2000,101:1409-1417) which involves mapping of arrhythmogenic activity exiting from specific sites in the left atrium, and isolation of those sites. With that technique, focal breakthrough is the most common failure mechanism that permits late organized tachycardias to develop, as is shown in this paper. The approach of isolation of only arrhythmogenic pulmonary veins however, can be problematic. These arrhythmogenic foci are frequently not reproducible. Permanent electrical isolation may be difficult. Ablation at or beyond the pulmonary veins may be associated with late pulmonary vein stenosis. Because of these limitations, other techniques have been developed. One technique is antral isolation in which the isolating ablation lesions are placed further from the pulmonary veins. An alternate technique proposed by Pappone and colleagues (Circulation. 2000;102:2619-2628) uses circular linear lesions that encompass, but are far from, the pulmonary ostia. These latter techniques also can be associated with recurrent left atrial tachycardias or left atrial flutter, however, in these situations, the placement of the lesions favors macroreentrant circuits rather than focal recurrences. These are often difficult to map and ablate, and usually require linear lesions in the left atrium rather than focal lesions within the veins.
One fact that must be considered in papers such as this is that recurrent atrial arrhythmias are relatively common in the first 6 to 8 weeks after any ablation procedure for atrial fibrillation. Most authors recommend drug therapy if needed for symptom control during this period to allow for atrial scarring from the ablation to become complete before attempting a repeat ablation procedure. Since these rhythms may sometimes be quite difficult to manage, postponing a repeat ablation may represent a clinical dilemma that may not be easy to deal with. However, some of these recurrent atrial arrhythmias will disappear over time, and it is worth trying to wait for at least 6 months before attempting a repeat ablation.
The techniques for catheter ablation of atrial fibrillation continue to evolve. There are still significant limitations for these procedures, but progress is being made.
Dr. DiMarco, Professor of Medicine, Division of Cardiology, University of Virginia, Charlottesville, is on the Editorial Board of Clinical Cardiology Alert.