Ablation of Ventricular Arrhythmias

Abstract & Commentary

Synopsis: Triggering ventricular premature beats from distal Purkinje fibers or the right ventricular outflow tract are critical initiating factors in patients with VF associated with the long QT and Brugada syndromes. Elimination of these focal triggers can provide relief from recurrent arrhythmias.

Source: Haissaguerre M, et al. Circulation. 2003;108:925-928.

Haissaguerre and colleagues report a new technique for managing frequent arrhythmias in patients with syndromes characterized by abnormal ventricular repolarization. They describe the results of mapping and ablation of ventricular premature beats in 7 patients. Four patients with long QT syndromes (LQTS) and 3 patients with Brugada syndrome are included in the study. Each patient had presented with 1 or more documented episodes of ventricular tachycardia or ventricular fibrillation (VF). The mean number of episodes were 14 ± 8 for the 2 Brugada syndrome patients and 6 ± 4 for the LQTS patients. Although each LQTS patient had a corrected QTc interval of greater than 460 msec, they did not have known KCNQ1, SCN5A, or HERG channelopathies found during genetic testing. The 3 Brugada syndrome patients had the classic ST segment elevation and abnormal QRS complex associated with that disorder. One of these patients had a familial SCN5A channelopathy. No patient had structural heart disease. Five patients had implantable cardioverter defibrillators in situ. Patients were hospitalized within 2 weeks of their most recent episode of VF. In-hospital monitoring documented frequent ventricular premature beats (11,559 ± 13,111 per 24 hours). Triggering premature beats were documented at the time of initiation of VF by either ambulatory monitoring or stored defibrillator electrograms. Triggering premature beats were found to be either monomorphic or polymorphic. All patients underwent electrophysiologic study with right and left ventricular mapping. In the 4 patients with LQTS, 1 patient had premature beats originating from the right ventricular outflow tract, 2 patients had polymorphic ventricular premature beats arising from the peripheral arborization of Purkinje fibers in the left ventricle, and 1 patient’s premature beats originated from the posterior fascicle. Before each target premature beat, a Purkinje potential preceded the local endocardial muscle activation by an interval of 34 ± 17 msec. Variations in conduction delay between the Purkinje potential and the local myocardium were seen during repetitive activity. A radiofrequency application at the site of origin of these beats produced temporary exacerbations of arrhythmia followed by disappearance of spontaneous ventricular ectopy. Twelve to 24 minutes of radiofrequency energy application were required for elimination of all premature beats.

In the patients with Brugada syndrome, sites of origin in the right ventricular outflow tract and right ventricular Purkinje fibers were ablated after mapping. In 1 of these patients, Purkinje potentials were identified. In the 2 patients who had inducible VF prior to ablation, no VF was inducible after ablation.

During a mean follow-up of 17 ± 17 months, there were no recurrences of VF, syncope, or sudden death in any patient. Two patients were maintained on beta-blockers, while the remaining 5 patients were followed without antiarrhythmic drug therapy.

Haissaguerre et al concluded that triggering ventricular premature beats from distal Purkinje fibers or the right ventricular outflow tract are critical initiating factors in patients with VF associated with the long QT and Brugada syndromes. Elimination of these focal triggers can provide relief from recurrent arrhythmias.

Comment by John DiMarco, MD, PhD

Haissaguerre et al previously reported successful mapping and ablation of focal triggers arising from the Purkinje fiber network in patients with idiopathic VF.1 The patients in that report had normal electrocardiograms at baseline and no evidence for structural heart disease. This paper extends this approach to patients with abnormalities of repolarization on resting electrocardiograms that are diagnostic of either the LQTS or Brugada syndrome.

One must remain cautious about accepting, generalizing, and applying these findings. If these patients truly had LQTS or Brugada syndrome, they should have persistent problems of repolarization in diffuse areas of the myocardium, which place them at continued risk for life-threatening arrhythmias. Although eliminating focal triggers might decrease the short-term occurrence of life-threatening ventricular arrhythmias, it is premature to conclude that this will provide a long-term cure. Ablation of focal sources should not affect the basic underlying mechanism, and it is unknown if more ventricular premature beats will be seen with longer follow-up.

In this regard, it is noteworthy that the patients with LQTS did not have evidence for the 3 most common ion channel disorders associated with this disorder. Whether this approach would be effective in LQTS patients with the more common ion channel mutations remains to be shown.

It is also striking that the patients with Brugada syndrome had a change in the response to stimulation after the focal ablation. One would have guessed that programmed stimulation, which provides premature beats, would still be able to initiate arrhythmias since the repolarization abnormality in the right ventricle should still be present. The reason why focal ablation would affect this response is unexplained by this paper. If the observation is confirmed, it raises questions about our current understanding of the mechanism responsible for arrhythmias in patients with Brugada syndrome.

Dr. DiMarco, Professor of Medicine, Division of Cardiology, University of Virginia, Charlottesville, is on the Editorial Board of Clinical Cardiology Alert.

Reference

1. Shimoni S, et al. Circulation. 2002;106:950-967.