OBJECTIVES: This study assessed the useful role of intracardiac mapping and radiofrequency catheter ablation in eliminating drug-refractory monomorphic ventricular ectopic beats in severely symptomatic patients. BACKGROUND: Ventricular ectopic activity is commonly encountered in clinical practice. Usually, it is not associated with life-threatening consequences in the absence of significant structural heart disease. However, frequent ventricular ectopic beats can be extremely symptomatic and even incapacitating in some patients. Currently, reassurance and pharmacologic therapy are the mainstays of treatment. There has been little information on the use of catheter ablation in such patients. METHODS: Ten patients with frequent and severely symptomatic monomorphic ventricular ectopic beats were selected from three tertiary care centers. The mean frequency +/- SD of ventricular ectopic activity was 1,065 +/- 631 beats/h (range 280 to 2,094) as documented by baseline 24-h ambulatory electrocardiographic (ECG) monitoring. No other spontaneous arrhythmias were documented. These patients had previously been unable to tolerate or had been unsuccessfully treated with a mean of 5 +/- 3 antiarrhythmic drugs. The site of origin of ventricular ectopic activity was accurately mapped by using earliest endocardial activation time during ectopic activity or pace mapping, or both. RESULTS: During electrophysiologic study, no patient had inducible ventricular tachycardia. The ectopic focus was located in the right ventricular outflow tract in nine patients and in the left ventricular posteroseptal region in one patient. Frequent ventricular ectopic beats were successfully eliminated by catheter-delivered radiofrequency energy in all 10 patients. The mean number of radiofrequency applications was 2.6 +/- 1.3 (range 1 to 5). No complications were encountered. During a mean follow-up period of 10 +/- 4 months, no patient had a recurrence of symptomatic ectopic activity, and 24-h ambulatory ECG monitoring showed that the frequency of ventricular ectopic activity was 0 beat/h in seven patients, 1 beat/h in two patients and 2 beats/h in one patient. CONCLUSIONS: Radiofrequency catheter ablation can be successfully used to eliminate monomorphic ventricular ectopic activity. It may therefore be a reasonable alternative for the treatment of severely symptomatic, drug-resistant monomorphic ventricular ectopic activity in patients without significant structural heart disease.
OBJECTIVES: This study assessed the useful role of intracardiac mapping and radiofrequency catheter ablation in eliminating drug-refractory monomorphic ventricular ectopic beats in severely symptomatic patients. BACKGROUND: Ventricular ectopic activity is commonly encountered in clinical practice. Usually, it is not associated with life-threatening consequences in the absence of significant structural heart disease. However, frequent ventricular ectopic beats can be extremely symptomatic and even incapacitating in some patients. Currently, reassurance and pharmacologic therapy are the mainstays of treatment. There has been little information on the use of catheter ablation in such patients. METHODS: Ten patients with frequent and severely symptomatic monomorphic ventricular ectopic beats were selected from three tertiary care centers. The mean frequency +/- SD of ventricular ectopic activity was 1,065 +/- 631 beats/h (range 280 to 2,094) as documented by baseline 24-h ambulatory electrocardiographic (ECG) monitoring. No other spontaneous arrhythmias were documented. These patients had previously been unable to tolerate or had been unsuccessfully treated with a mean of 5 +/- 3 antiarrhythmic drugs. The site of origin of ventricular ectopic activity was accurately mapped by using earliest endocardial activation time during ectopic activity or pace mapping, or both. RESULTS: During electrophysiologic study, no patient had inducible ventricular tachycardia. The ectopic focus was located in the right ventricular outflow tract in nine patients and in the left ventricular posteroseptal region in one patient. Frequent ventricular ectopic beats were successfully eliminated by catheter-delivered radiofrequency energy in all 10 patients. The mean number of radiofrequency applications was 2.6 +/- 1.3 (range 1 to 5). No complications were encountered. During a mean follow-up period of 10 +/- 4 months, no patient had a recurrence of symptomatic ectopic activity, and 24-h ambulatory ECG monitoring showed that the frequency of ventricular ectopic activity was 0 beat/h in seven patients, 1 beat/h in two patients and 2 beats/h in one patient. CONCLUSIONS: Radiofrequency catheter ablation can be successfully used to eliminate monomorphic ventricular ectopic activity. It may therefore be a reasonable alternative for the treatment of severely symptomatic, drug-resistant monomorphic ventricular ectopic activity in patients without significant structural heart disease.