Reversal of Cardiomyopathy in Patients With Repetitive Ventricular Ectopy

Abstract & Commentary

By John P. DiMarco, MD, PhD Dr. DiMarco is Professor of Medicine, Division of Cardiology, University of Virginia, Charlottesville. Dr. DiMarco is a consultant for Novartis and does research for Medtronic and Guidant.

Synopsis: Arrhythmia is the primary problem rather than a marker of an underlying cardiomyopathy.

Source: Yarlagadda RK, et al. Reversal of Cardiomyopathy in Patients with Repetitive Monomorphic Ventricular Ectopy Originating from the Right Ventricular Outflow Tract. Circulation. 2005;112:1092-1097.

Yarlaggada and colleagues report on 27 consecutive patients with repetitive monomorphic ventricular ectopy who underwent radiofrequency catheter ablation over a 4-year period from April 2000 to December 2004. Patients with sustained ventricular tachycardia or frequent nonsustained runs of ventricular tachycardia were excluded. At baseline, a 24-hour ambulatory ECG was used to quantify the amount of ventricular ectopy. Cardiac structure and function were assessed with cardiac magnetic resonance imaging and echocardiography.

All patients underwent electrophysiologic study. Three dimensional mapping of the right ventricle was performed during periods of spontaneous ventricular ectopy using either a contact (CARTO XP) or noncontact (Endocardial Solutions, Inc.) electroanatomic mapping system. Radiofrequency ablation was performed using a 4mm tipped catheter. Ablation sites were selected based on electroanatomic mapping and confirmed by pace mapping. After ablation, all patients underwent repeat 24-hour Holter monitoring within 3 months, and left ventricular function was assessed at that time.

The study population consisted of 27 patients (11 men and 16 women) with a mean age of 47 ± 15 years. At baseline, 19 had ejection fractions greater than 45%, and 8 patients had ejection fractions ≥ 45%. Antiarrhythmic drug therapy had been tried unsuccessfully in 19 patients but, in the remaining 10 patients, catheter ablation was the initial treatment selected. During baseline 24 hour ambulatory ECG monitoring, patients had a mean of 17, 624 + 12,611 ventricular premature beats. This represent- ed 2% to 44% of the patients daily cardiac cycles. Sustained monomorphic ventricular tachycardia could be induced with isoproterenol in only 2 of 27 patients. Sustained ventricular tachycardia was not inducible with programmed stimulation in any patient. Four patients, however, manifested sustained ventricular fibrillation in response to triple ventricular extrastimuli.

In 21 patients, there was a single ectopic ECG pattern which had a left bundle branch, inferior axis morphology, while 6 patients had a similar dominant focus, but other morphologies were identified. Radiofrequency ablation was successful in 23 of 27 patients, including 7 of the 8 patients with left ventricular ejection fractions ≥ 45% at baseline. Patients with depressed left ventricular function were more likely to be older than patients with normal function. Site of ectopy origin did not influence function. Patients with and without normal function most frequently had their ectopy arising from the posterior or posterior septal wall of the right ventricular outflow tract. Radiofrequency ablation was successful in 7 of the 8 patients with depressed ventricular function. In these 7 patients, there was a reduction in ventricular ectopy from a baseline of 17,549 ± 11,479 beats per 24 hours to 507 ± 722 beats for 24 hours after ablation. The left ventricular ejection fraction increased from 39 ± 6% to 62 ± 6%, a median of 3 months after ablation. A single patient with depressed left ventricular function at baseline who did not have a successful ablation had only a minor change in the ejection fraction after the procedure.

Yarlagadda and colleagues conclude that very frequent ventricular ectopy may lead to reversible left ventricular dysfunction. They argue that since older patients are more likely to have left ventricular dysfunction, that patients with this frequent ectopy who are medically managed should be carefully followed over time. Since elimination corrects the ventricular dysfunction, the data argue that the arrhythmia is the primary problem rather than a marker of an underlying cardiomyopathy.


The management of patients with frequent ventricular ectopy and no identifiable structural heart disease can be quite controversial. Many of these patients have long or nearly continuous runs of ventricular bigeminy and are highly symptomatic even if they are free of runs of nonsustained or sustained ventricular tachycardia. Conventional antiarrhythmic drug therapy is frequently unsuccessful. Beta blockers may actually make things worse by slowing the effective ventricular rate during episodes of bigeminy. In this paper, Yarlagadda et al show that some patients with very frequent ventricular ectopy may also develop a reversible cardiomyopathy that can be corrected by eliminating the ventricular ectopy. It is often difficult in a patient with left ventricular dysfunction and ectopy to know which comes first, the cardiomyopathy or the ventricular arrhythmia. Data presented here would suggest that patients with this extreme amount of ventricular ectopy should undergo a trial of catheter ablation, particularly if only a single morphology of ectopy is noted during monitoring. In at least some patients, the arrhythmia may be the primary problem, one that can be eliminated with catheter ablation.