Premature Ventricular Contractions May Not Be All That Benign: The Role of Radiofrequency Ablation

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Mujeeb Sheikh, MD; Steven R. Bruhl, MD, MS; Warren Foster, MD; Blair Grubb, MD, FACC; Yousuf Kanjwal, MD, FACC
Department of Cardiology, Section of Cardiac Electrophysiology, University of Toledo Medical Center, Toledo, Ohio

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In this article, the authors present a case study and overview on the treatment of premature ventricular contractions.

Index Case

A 22-year-old female was referred to our clinic for the evaluation of symptomatic premature ventricular contractions (PVCs). The patient had been experiencing fatigue, shortness of breath, frequent palpitations, and exercise intolerance for the last 5 years. Her past medical history was otherwise unremarkable, including no sudden death in the family. Further, she reported that the beta blockers and lifestyle modification had failed to resolve her symptoms. A review of 24-hour Holter monitoring demonstrated a total burden of 25,000 PVCs with left bundle morphology, in bigeminal and trigeminal pattern.

Two-dimensional echocardiogram revealed reduced left ventricular systolic function, with an estimated ejection fraction of 40–45% without wall motion or valvular abnormalities. Her ischemic workup was also negative. Magnetic resonance imaging showed no evidence of right ventricular (RV) dysplasia. In view of the increased burden of symptomatic PVCs and left ventricular systolic dysfunction, as well as no response to medication, she was considered for radiofrequency (RF) ablation.

Baseline electrophysiologic procedure was performed in the EP lab. After obtaining proper consent, sheaths were placed in both left and right femoral veins. A non-contact mapping system (Multi-electrode Array balloon, St. Jude Medical, St. Paul, MN) was used, and for making a 3-D map we used a 7 French, 4-mm-tip, standard curve EPT catheter (Boston Scientific, Natick, MA). The patient had multiple unifocal PVCs at baseline. Surface electrocardiogram was suggestive of PVC morphology with right ventricular outflow tract (RVOT) morphology and with possible origin near the septal portion of the RVOT. We initially tried to induce sustained ventricular tachycardia (VT) by ventricular stimulation protocol from the RV apex and outflow tract with basic 2 cycle lengths and up to 3 extrastimuli at baseline and on Isuprel. Three-dimensional mapping was performed, and looking at the activation map, the earliest activation of PVCs was found at the posteroseptal region of the RVOT (Figure 1). Further confirmation was provided by pace mapping from the same site, which produced a perfect 12/12 match. After mapping a number of PVCs and determining the earliest activation and breakout, RF ablation was performed. Multiple RF lesions were given at that particular area, and there was immediate termination of the PVCs. After waiting for more than half an hour as well as repeating the ventricular stimulation protocol on Isuprel, no PVCs were seen. At one-month and six-month follow-up, the patient underwent Holter monitoring and had no PVCs recorded. Follow-up echocardiogram showed complete normalization of her ejection fraction as well as resolution of her symptoms.

Radiofrequency Ablation of Premature Ventricular Complexes

Isolated PVCs are the most frequent arrhythmias encountered in clinical practice. In the Framingham Offspring Study of patients with structurally normal hearts, PVCs were reported in 27% of patients during exercise.1 In symptomatic patients, frequent PVCs are associated with reduced quality of life, increased outpatient visits, repeated electrocardiographic (ECG) and Holter monitoring, increased medication side effects, and substantial consumption of health services. Frequent PVCs are associated with increased risk of sudden cardiac death from lethal arrhythmias and lead to left ventricular dysfunction.2,3 RF catheter ablation is an established, effective and curative therapy for VTs in structurally normal hearts. More recently, ablation has emerged as a promising first-line therapy for symptomatic PVCs originating either from the right or left ventricle in structurally normal or abnormal hearts.4

Electrophysiologically, PVCs are early depolarization due to increased automaticity. PVCs can be epicardial or endocardial in origin, and more common in the right ventricle as compared to the left ventricle. Ectopy arising from the right ventricle has left bundle morphology, whereas right bundle morphology recognizes left ventricular origin of PVC on a surface electrocardiogram. Within the right ventricle they can originate from the apex, septum and RVOT. Several electrocardiographic algorithms have been developed to identify the site of origin of PVCs from different foci in right and left ventricle.5

PVC and Arrhythmic Risk

The frequency of PVCs is influenced by the autonomic tone, electrolyte disturbances and ischemia. A major concern is that PVCs may initiate VT, polymorphic VT and ventricular fibrillation. Monomorphic VT can be re-entry or due to triggered activity. Right ventricular outflow tract VT is a triggered VT that has a characteristic LBBB pattern in V1 and inferior axis on a surface electrocardiogram. Idiopathic RVOT in the structurally normal heart has excellent prognosis, is catecholamine sensitive and is often induced with exercise or infusion of catecholamine, such as isoproterenol and epinephrine. Radiofrequency catheter ablation has become a primary therapy for idiopathic VT originating from the RVOT; the success rates are approximately 90%, with low recurrence rates. Precise localization of the VT origin in the RVOT for radiofrequency catheter ablation is determined by the combined use of pace mapping during sinus rhythm and activation mapping during VT or PVC in electrophysiological studies. On the other hand, PVC with short coupling extrasystoles can initiate polymorphic VT and ventricular fibrillation. Haissaguerre et al6 were the first to demonstrate that PVCs initiating idiopathic VF could be localized. They recruited 27 patients who were resuscitated from recurrent episodes of primary idiopathic VF. In all 27 patients, the first initiating PVCs were observed during the electrophysiologic studies and successfully mapped. For these 27 patients, PVCs were successfully eliminated by RF catheter ablation. In patients with an underlying substrate for ventricular fibrillation, PVC ablation can be successfully performed, but generally require a back-up ICD.

PVC and Left Ventricular Systolic Dysfunction

Atrial fibrillation and other supraventricular arrhythmias are well known to be associated with reduced left ventricular function. More recently, the increased burden of PVC has been shown to cause tachycardia-induced cardiomyopathy. In one retrospective study of 108 patients that evaluated burden of PVC with frequency of the left ventricular dysfunction, 24 patients had <1,000 PVCs/24 hours, 55 patients had 1,000–10,000 PVCs/24 hours, and 29 patients had ≥10,000 PVCs/24 hours. The prevalence of left ventricular dysfunction was 4%, 12%, and 34%, respectively (p = 0.02).7 Oftentimes it is difficult to differentiate between primary cardiomyopathy and tachycardia-induced cardiomyopathy. Reversal of cardiomyopathy after radiofrequency ablation or suppression of medication is the only reliable way to differentiate the two etiologies. In another study of 60 patients comparing LV ejection fraction before and after PVC ablation, LV function normalized in 18 (82%) of 22 patients from a baseline of 34% to 59% ± 7% (p < 0.0001) within six months.8 On the other hand, in patients with normal baseline ejection fraction, RF ablation is associated with improved exercise tolerance, reduction in LV and RV dimensions, and reduction in radial and longitudinal strain.9

Risk Stratification and Selection of Patients for Ablation

Selection of patients for PVC ablation requires a comprehensive evaluation that includes surface ECG and Holter monitoring in order to document burden of PVCs, associated symptoms during these episodes and morphological features of PVC. An echocardiogram and stress test may be necessary to evaluate coronary ischemia and left ventricular systolic function. Additional diagnostic testing, including electrophysiologic studies, cardiac magnetic resonance angiography, and coronary angiography, should be considered in appropriate clinical circumstances. Further, secondary causes of increased frequency of ventricular ectopy, including electrolyte imbalance, caffeine, alcohol, or medication, need to be considered and treated first. Generally, symptomatic patients with increased burden of PVC, medication intolerance, and PVC-induced cardiomyopathy should be considered for RF ablation.

Management of Symptomatic PVCs

Lifestyle modification should be considered as an initial step in the management of patients with symptomatic PVCs. Medical therapy, usually in form of beta blockers, is the first-line therapy for suppression of symptomatic PVCs; besides being inexpensive and tolerable,10 there is substantial evidence supporting the use of beta blockers in patients with coronary artery disease (CAD) and heart failure to reduce mortality and sudden cardiac death. However, as much as beta blockers are a reasonable choice, they may not provide curative therapy for symptomatic PVC.

The use of antiarrhythmic agents, particularly class I (flecainide, encainide), tend to be restricted due to proarrhythmic concerns in patients with coronary artery disease. In high-risk patients, such as those with structural heart disease and CAD, amiodarone and dofetilide provide acceptable alternative or adjunctive therapies to suppress ventricular arrhythmia ectopy.11,12 Nevertheless, the concerns of adverse effects with these medications preclude their long-term use for suppression of ventricular ectopy.

Radiofrequency Ablation

Radiofrequency ablation provides a definite therapy for symptomatic PVCs. In addition to an excellent safety profile, ablation has been associated with reversal of ventricular dysfunction, improvement in symptoms, exercise tolerance and reduction of ICD shocks. While the surface ECG has good predictive value in localization of these foci, the exact localization is usually accomplished by pace mapping and activation mapping. In activation mapping, the site of ectopic beats is determined by the exact time the local myocardium is depolarized as compared to a standard reference point. By combining relative activation time with the location of each point on an electroanatomic map, a three-dimensional map of cardiac activation is created. Color-coded lines help to determine the propagation wave. Successful ablation sites show presystolic potential, which are local electrograms before QRS. In pace mapping, the captured QRS from the pacing site is compared to baseline 12-lead ECG, and if there is complete match, the focal site is identified and ablated. Advanced electroanatomic mapping has been developed that use cardiac imaging from CT, MRI or ultrasound to aid in the construction of chamber geometry and provide a precise location of the points of interest.

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