Aggressive Ablation for SVT

ABSTRACT & COMMENTARY

Synopsis: Empiric slow pathway catheter ablation appears beneficial in patients who have spontaneous tachycardias and dual AV nodal pathway physiology, despite the fact that these arrhythmias may not be reproducible at electrophysiologic study.

Source: Lin JL, et al. J Am Coll Cardiol 1998;31: 855-860.

Lin and colleagues evaluated the long-term efficacy of an empiric slow atrioventricular (AV) nodal pathway catheter ablation in patients with spontaneous documented paroxysmal supraventricular tachycardia (PSVT) in whom PSVT could not be induced during baseline electrophysiologic study. Lin et al reviewed data from a series of 520 patients who received radiofrequency catheter ablation for AV nodal reentrant tachycardia at their institutions. Among these, there were 27 patients who had at least one electrocardiographically documented episode of PSVT but did not have the rhythm induced during EP study. Two control groups were also analyzed. One group consisted of 55 patients with clinical and inducible AV nodal reentrant tachycardia. The third group consisted of 47 patients who had other clinically documented arrhythmias but also had dual AV nodal pathway physiology in response to programmed atrial stimulation. The authors' stimulation protocol included single and double atrial extrastimuli and rapid atrial pacing both under baseline conditions and after isoproterenol and, if necessary, atropine infusions. Radiofrequency catheter ablation was carried out using standard techniques in patients with both suspected and documented AV nodal reentrant tachycardia. The end point for catheter ablation was the disappearance of dual AV nodal pathway physiology and AV nodal echo beats after the final ablation. Follow-up was conducted in the first group of patients at monthly intervals. The frequency of PSVT recurrence was analyzed in the patients in the first group according to whether an attempted radiofrequency ablation was performed. Data from the first group, both electrophysiologic and follow-up, were compared with data from the two comparison groups.

There were 27 patients in the group with suspected AV nodal reentrant tachycardia who did not have inducible tachycardia in the laboratory. All of these patients had a 12-lead electrocardiogram that was consistent with AV nodal reentry. The frequency of PSVT attacks was 4 ± 3 times per year. This was lower than the frequency among the patients with inducible AV nodal reentry, 10 ± 11 times per year. Patients without inducible tachycardia had only minor changes in the electrophysiologic properties between their slow and fast pathways for both antegrade and retrograde conduction. Of the 27 patients in the group without inducible SVT, 16 patients went on to an attempt at catheter ablation and 11 declined such an attempt. During the follow-up period, none of the 16 patients who received an empiric slow pathway catheter ablation had recurrence of clinical tachycardia. In contrast, seven of the remaining 11 patients had recurrence of PSVT during 13 ± 14 months of follow-up.

Lin et al conclude that empiric slow pathway catheter ablation appears beneficial in patients who have spontaneous tachycardias and dual AV nodal pathway physiology, despite the fact that these arrhythmias may not be reproducible at electrophysiologic study.

COMMENT BY JOHN P. DiMARCO, MD, PhD

Currently, the success rate for radiofrequency ablation of the slow AV nodal pathway in patients with AV nodal reentrant tachycardia is high, and the complication rate is low. This procedure has become the treatment of choice for patients with recurrent symptomatic episodes of supraventricular tachycardia. This paper deals with one of the dilemmas in the application of such therapy. There are occasional patients with documented episodes of narrow complex tachycardia in whom no sustained tachycardia can be induced in the laboratory. The approach outlined by Lin et al for this situation seems reasonable. Every patient in their series had a documented sustained tachycardia with a 12-lead electrocardiogram. This makes the possibility of another mechanism of tachycardia unlikely. This cannot be said for many clinical situations, where the only evidence of tachycardia available is the patient's own history of symptoms or just a rhythm or monitor strip. Histories are notoriously unreliable about the mechanism of tachycardia, and monitor strips do not provide enough information to exclude other mechanisms of tachycardia, including sinus tachycardia. If, however, a 12-lead electrocardiogram has been obtained during tachycardia, it does seem reasonable to use the documentation of dual AV nodal physiology as enough evidence to proceed to catheter ablation. Catheter ablation in this area is safe. If one avoids ablating high on the septum, the risk of AV block is less than one in 300-500 cases. Other major complications are similarly rare with this procedure. However, the operator must remember that up to 30% of patients will have dual AV nodal physiology, defined as a 50 msec jump in the AH interval with a 10 msec decrement in the premature interval. Therefore, it was important for Lin et al to include their second control group of patients with dual AV nodal physiology who had only other arrhythmias documented clinically and at EP study. These patients had no episodes of PSVT during follow-up, even though no slow pathway ablations were performed.

The treatment algorithm should, therefore, be an initial attempt to document the arrhythmia. If the patient has not had full electrocardiographic documentation of the arrhythmia, I would then be reluctant to proceed with an ablation unless PSVT could be initiated. The possible exception would be patients who had multiple echo beats that were clearly AV nodal in origin but no long runs of tachycardia. For the patient with a single echo beat or with just a jump in the AH interval, I would prefer to discharge the patient, follow him, and try to document an episode electrocardiographically. Even though the risk of slow pathway ablation is relatively low, I do not think one should do this without some supporting evidence that the patient is likely to have AV node reentry.