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Advances in Arrhythmia and Electrophysiology Premature Ventricular Contraction-Induced Cardiomyopathy A Treatable Condition Yong-Mei Cha, MD; Glenn K. Lee, MBBS; Kyle W. Klarich, MD; Martha Grogan, MD P measured by the LV ejection fraction (LVEF) and LV end-diastolic dimension over a follow-up period of 4 to 8 years (Figure 1). Downloaded from http://circep.ahajournals.org/ by guest on November 20, 2016 remature ventricular contractions (PVCs) are early depolarizations of the myocardium originating in the ventricle. They are often seen in association with structural heart disease and represent increased risk of sudden death,1 yet they are ubiquitous, even in the absence of identifiable heart disease.1,2 They may cause troubling and sometimes incapacitating symptoms such as palpitations, chest pain, presyncope, syncope, and heart failure.3 Traditionally, they have been thought to be relatively benign in the absence of structural heart disease.4,5 Over the last decade, however, PVC-induced cardiomyopathy has been a subject of great interest and the evidence for this entity is rapidly emerging. Electrophysiological Characteristics PVC Burden Several studies have shown that the frequency of PVCs correlates at least modestly with the extent of LV dysfunction and ventricular dilation at the time of initial clinical presentation.13–17 Patients with decreased LVEF had a higher mean PVC burden than their counterparts with normal LV function (29%–37% versus 8%–13%).15,18,19 However, there are no clear-cut points that mark the frequency at which cardiomyopathy is unavoidable. Niwano et al13 used a cut point of 20 000 PVCs over 24 hours to define the high-frequency group, whereas Kanei et al17 used a figure of 10 000 PVCs per day. Other studies defined “frequent” PVCs as ⬎10% of total beats rather than the absolute number of PVCs,18,19 yet in some cases, a high PVC burden may not impair LV function, whereas PVC-induced cardiomyopathy can be observed in patients with lower PVC frequencies, albeit at lower incidences.12,16,17 It is not known why the majority of patients with frequent PVCs have a benign course, whereas up to one third of them develop cardiomyopathy. One possible explanation is that the evaluation of PVC burden using 24-hour Holter monitoring may be inadequate and may misrepresent the patient’s true PVC burden.20 Baman et al18 suggested that a PVC burden of ⬎24% had a sensitivity and specificity of 79% and 78%, respectively, in separating the patient populations with impaired versus preserved LV function. Nevertheless, the majority of patients presenting with frequent PVCs had preserved LVEF.4,9,12,13,15 Therefore, although significant, the PVC burden is not the only factor contributing to impairment of LV systolic function.9,15,21 Epidemiology PVCs are common with an estimated prevalence of 1% to 4% in the general population.5 In a normal healthy population, PVCs have been detected in 1% of subjects on standard 12-lead electrocardiography and between 40% and 75% of subjects on 24- to 48-hour Holter monitoring.6 Their prevalence is generally age-dependent,1 ranging from ⬍1% in children ⬍11 years7 to 69% in subjects ⬎75 years.8 Commonly thought to be a benign entity,4,5 the concept of PVC-induced cardiomyopathy was proposed by Duffee et al9 in 1998 when pharmacological suppression of PVCs in patients with presumed idiopathic dilated cardiomyopathy subsequently improved left ventricular (LV) systolic dysfunction. Many of these patients often have no underlying structural heart disease and subsequently develop LV dysfunction and dilated cardiomyopathy; in cases of those with an already impaired LV function from underlying structural heart disease, worsening of LV function may occur.10,11 The exact prevalence of PVC-induced cardiomyopathy is not known; it is an underappreciated cause of LV dysfunction, and it is primarily observed in older patients.12 This observation could be due to the fact that the prevalence of PVCs increases with age or the possibility that PVC-induced cardiomyopathy develops in a time-dependent fashion.12 In fact, Niwano et al13 demonstrated progressive worsening of LV function in patients with frequent PVCs (⬎1000 beats/day) as PVC Origin Approximately two thirds of idiopathic PVCs originate from the ventricular outflow tracts, primarily the right ventricular outflow tract.3,22 The ventricular outflow tract musculature, Received March 8, 2011; final revision received October 26, 2011; accepted October 31, 2011. From the Division of Cardiovascular Diseases (Y.-M.C., K.W.K., M.G.), Mayo Clinic, Rochester, MN; and the Department of Medicine (G.K.L.), National University Health System, Singapore. Guest Editor for this article was Kenneth A. Ellenbogen, MD. Correspondence to Yong-Mei Cha, MD, Division of Cardiovascular Diseases, Mayo Clinic, 200 First Street SW, Rochester, MN 55905. E-mail [email protected] (Circ Arrhythm Electrophysiol. 2012;5:229-236.) © 2011 American Heart Association, Inc. Circ Arrhythm Electrophysiol is available at http://circep.ahajournals.org 229 DOI: 10.1161/CIRCEP.111.963348 230 Circ Arrhythm Electrophysiol February 2012 Downloaded from http://circep.ahajournals.org/ by guest on November 20, 2016 Figure 1. Relationship between the prevalence of premature ventricular contractions (PVCs) and changes in left ventricular ejection fraction (LVEF) and left ventricular end-diastolic dimension (LVEDD) over a 4-year observational period. The ⌬LVEF was calculated as (LVEF at the evaluation time point)⫺(initial LVEF) and the ⌬LVEDD was calculated as (LVEDD at the evaluation time point)⫺(initial LVEDD); each parameter was plotted against the PVC prevalence for each patient. Although most of the patients exhibited only small changes in LVEF and LVEDD, several patients exhibited a relatively large decrease in the LVEF and increase in the LVEDD. There was a weak but significant negative correlation between the PVC prevalence and ⌬LVEF and a weak but significant positive correlation between the PVC prevalence and ⌬LVEDD at the 4-year follow-up. Adapted from Niwano et al.13 Used with permission. and hence the anatomic source of the PVCs, may extend above the pulmonary or aortic valves. Gami et al23 examined 603 autopsy hearts and found that 57% of these hearts had myocardial extensions above the aortic valve, and 74% had extensions above the pulmonary valve. Extensions were noted more often in the right coronary cusp (55%) than in the left coronary cusp (24%) and noncoronary/posterior cusp (⬍1%). In contrast, myocardial extensions above the 3 pulmonary cusps are distributed more evenly (45%– 60%). These myocardial extensions constitute the electric substrates for ectopies and tachycardia. The remaining third of PVCs may have various ventricular origins, including the ventricular free walls, LV fascicles, septum, and papillary muscles. These ectopics may originate from single or multiple foci, presenting as monomorphic or polymorphic PVCs on electrocardiography. It should be noted that PVCs originating from the outflow tracts are often monomorphic. Munoz et al22 retrospectively studied 70 subjects who underwent PVC ablation. Of these, 17 (24%) had a reduced LVEF ⬍50%. When compared with those with LVEF of ⱖ50%, there was no significant difference in baseline patient characteristics except that patients with reduced LVEF were less likely to have reported symptoms. Interestingly, in addition to a higher PVC burden being observed in patients with reduced LVEF, PVCs originating from the right ventricle were associated with significant reduction of LVEF at a PVC burden ⱖ10%, whereas PVCs originating from the LV were associated with significant reduction of LVEF only at a higher PVC burden of ⱖ20%. This finding, however, has to be interpreted within the constraints of a retrospective study design with a small sample size and a highly selected population. Whether delayed LV excitation and contraction from right ventricular PVCs pose greater hemodynamic threat to the myocardial function is a question that has not been studied, but it is plausible given the observation of right ventricular pacing-induced LV dysfunction.24 –29 PVC QRS Morphology, Duration, Coupling Interval, and Interpolation Although the threshold burden of PVCs associated with reduced LVEF was lower for right as compared with LV PVCs, data from 1 study suggest that the PVC morphology such as left bundle branch block or right bundle branch block pattern does not appear to affect the LVEF.22 However, the morphology can, to some extent, determine the site and etiology of the PVCs. PVCs with smooth and uninterrupted contours as well as a sharp QRS deflection typically represent an isolated ectopic focus and a structurally normal heart, whereas PVCs with broad notching and a slurred QRS deflection may represent a diseased myocardial substrate.30 PVCs originating from the fascicles or ventricular septum typically have a narrower QRS wave as opposed to PVCs originating from the free walls and outflow tracts. One study noted that PVC duration ⱖ140 ms was an independent predictor of impaired LVEF.22 There is inconsistent evidence as to whether the coupling interval is associated with LV dysfunction. A study by Sun et al31 reported that PVC coupling intervals ⱕ600 ms had a lower mean LVEF. A recent study by Olgun et al32 showed that PVC interpolation is an independent predictor of PVC-induced cardiomyopathy, although other studies have not corroborated this observation.22 These observations may not apply to all patients because these are single studies with small numbers of patients. Decreased PVC coupling interval may affect the LV filling profile, stroke volume, and pulse pressure.33 The association between coupling interval and hemodynamic/ structural consequence remains to be examined. Mechanisms and Pathophysiology PVC-induced cardiomyopathy was originally thought to be a type of tachycardia-induced cardiomyopathy,12,14,15,21 a phenomenon that has been well described in the context of atrial fibrillation, supraventricular tachycardia, and ventricular tachycardia.12 However, this concept has been called into question because patients with frequent PVCs have overall heart rates similar to those of their normal counterparts on Holter monitoring.13,14 The cellular mechanisms of PVCinduced cardiomyopathy have as yet not been elucidated and are only speculative at present given the dearth of animal models and prospective clinical studies in this area. However, on the basis of the observation that some patients with frequent PVCs had isoproterenol-facilitated induction of sustained monomorphic ventricular tachycardia of similar morphologies to the PVCs,34 Yarlagadda et al12 postulated that cAMP-mediated triggered activity may be an operative mechanism in some patients with PVCs. Frequent and persistent exposure to PVCs is associated with complex transient alterations in intracellular calcium and membrane ionic currents, heart rate dynamics, hemodynamic parameters, and both myocardial and peripheral vascular autonomic stimulation and inhibition.35–38 Morphological and functional abnormalities of the ventricular myocardium and outflow tracts may be found on MRI in patients with apparently idiopathic PVCs, albeit this does not necessarily have a clinical implication. Bogun et al15 postulated that ventricular dyssynchrony and increased oxygen consumption may be possible patho- Cha et al Premature Ventricular Contractions 231 Figure 2. Putative mechanisms of premature ventricular contraction (PVC)induced cardiomyopathy. Downloaded from http://circep.ahajournals.org/ by guest on November 20, 2016 genic mechanisms. Ventricular dyssynchrony results in compromised global cardiac mechanical efficiency, asymmetrically increased wall thickness in the late-activated regions, altered myocardial blood flow, and local changes in myocardial protein expression.28 The ventricular dyssynchrony associated with PVCs, particularly when the PVC burden is high, may contribute to LV dilation and impaired function in a fashion previously described for patients with left bundle branch block or chronic right ventricular pacing.25–29 Right ventricular pacing is notably associated with dyssynchronous ventricular contraction,39 changes in cardiac sympathetic activity, histopathology as well as ion channel expression and function40; animal models have shown that right ventricular pacing induces asymmetrical myocardial hypertrophy, myofibrillar disarray, and increased catecholamine concentrations in the myocardium.41– 43 Although clinical studies describe LV dysfunction developing over reasonably long periods of time (⬎4 years in the series of Niwano et al13), in canine models, LV dysfunction occurred within 4 to 12 weeks of induced ventricular ectopy.44,45 However, this PVC-induced cardiomyopathy animal model in a 3-month duration demonstrated the lack of myocardial fibrosis and absence of changes in apoptosis and mitochondrial function, which support a functional rather than structural mechanism. Smith et al46 observed sympathoexcitation evoked by acutely high rates of ventricular ectopy using programmed ventricular extrastimuli after every 4, 2, and 1 spontaneous sinus beats in patients with a history of supraventricular tachycardia. This inappropriate sympathetic activation could potentially impair LV function in the long-term, yet although animal models are crucial in helping us understand a variety of pathophysiological aspects that are difficult or unable to explore in human subjects, and give us an impression of the relationship between the onset and burden of PVCs to the development of systolic dysfunction, the limited comparability between animal and human studies has to be taken into account. Patient-specific factors such as genetic predispositions determining myocardial protein expression in response to PVC-induced stress may interact with PVC frequency to influence the risk of cardiomyopathy.47 The putative mechanisms of PVC-induced cardiomyopathy are summarized in Figure 2. Clinical Evaluation In many patients, the onset of frequent PVCs relative to the onset of LV dysfunction is unknown.47 It is particularly important to identify the primary disorder because of the potential reversibility of PVC-induced cardiomyopathy.48,49 Patients can present with debilitating symptoms, particularly palpitations, or other symptoms such as chest pain, presyncope, syncope, or heart failure manifested by decreased effort tolerance, possibly as a result of decreased effective cardiac output.3 The vast majority of these patients are healthy with no known structural heart disease,4 but a detailed family history is required to help exclude familial dilated cardiomyopathy. The physical examination findings are often normal except irregular heart rhythm when PVCs are frequent. The electrocardiography may indicate the presence and morphology of PVCs, but PVC burden should be assessed by continuous Holter monitoring for at least 24 hours. Because a single 24-hour recording may not reflect the true PVC load due to day-to-day variability, a strong suspicion that frequent PVCs may be the cause of LV dysfunction may warrant extended Holter recordings of 48 to 72 hours or several 24-hour Holter recordings.20 Echocardiography is useful to exclude valvular pathology, regional wall motion abnormalities, cardiomyopathies, or myocardial abnormalities such as noncompaction, all of which could be a cause for frequent PVCs. Echocardiographic features in PVC-induced cardiomyopathy include decreased LVEF, increased LV systolic and diastolic dimensions, wall motion abnormalities, which are often global as opposed to regional,20 as well as mitral regurgitation (typically due to mitral annular dilatation).14 Two-dimensional speckle tracking strain imaging has shown altered LV contractility, whereas the LVEF remains preserved.50 –54 Whether the abnormal findings from speckle tracking imaging predict the reduction of LVEF in patients 232 Circ Arrhythm Electrophysiol February 2012 Downloaded from http://circep.ahajournals.org/ by guest on November 20, 2016 Figure 3. Flow chart for the diagnosis, treatment and follow-up of patients presenting frequent premature ventricular contractions (PVCs). Electrocardiography indicates electrocardiography. LV indicates left ventricular; LVEF, left ventricular ejection fraction; PVC, premature ventricular contraction. with PVCs remains to be studied. Cardiac MRI may be warranted in detecting arrhythmogenic right ventricular cardiomyopathy with LV involvement and infiltrative disease when clinically suspected. Coronary angiography should be performed in every patient with reduced LV systolic function to exclude significant coronary artery disease except for those with a low cardiovascular risk. Appropriate workup should also be performed to exclude other causes of cardiomyopathy, including those related to drugs/toxins, infectious diseases, and endocrinopathies. It should be noted that PVC-induced cardiomyopathy remains a diagnosis of exclusion; underlying structural disease causing frequent PVCs must be ruled out. Given the reciprocal causal association between PVCs and cardiomyopathy where either 1 can lead to the other, it may be difficult to isolate the primary disorder.49,55 In many patients, the onset of frequent PVCs relative to the onset of LV dysfunction is unknown.47 It is particularly important to identify the primary disorder because of the potential reversibility of PVCinduced cardiomyopathy.48,49 Therapeutic Modalities A therapeutic medical trial or catheter ablation may be considered in patients with LV dysfunction and frequent PVCs (a generally accepted range of ⬎10 000 –20 00013,17 or ⬎10% of total heart beats18,19,22 over 24 hours) if the clinical suspicion for PVC-induced cardiomyopathy is high. The patient should be followed up over 3 to 12 months to assess posttreatment PVC frequency as well as LV size and function. The workup, treatment, and follow-up of patients with frequent PVCs are summarized in Figure 3. Pharmacological Therapy Because the long-term prognosis of frequent PVCs is generally considered to be benign and the majority of patients presenting with frequent PVCs have a preserved LVEF,4,9,12,13,15 the preferred treatment is usually reassurance and counseling of the patient with close follow-up if the patient is asymptomatic. In the presence of symptoms, pharmacotherapy such as a -blocker or a nondihydropyridine calcium channel blocker may be the first-line therapy.56 Krittayaphong et al57 showed, in a randomized placebo-controlled study, that atenolol significantly decreased symptom frequency and PVC count. Antiarrhythmics such as flecainide or sotalol may be considered when -blockers or calcium channel blockers are ineffective.58 Capucci et al59 demonstrated that 91% of patients taking flecainide and 55% of patients on mexiletine had a PVC reduction of ⱖ70%. In the presence of overt LV dysfunction, Class IA or IC drugs such as flecainide or propafenone are not recommended given their side effect Cha et al profiles, including the propensity for proarrhythmic effects and adverse impact on survival.3,60 Careful consideration in regard to the baseline renal and hepatic function is also necessary when initiating an antiarrhythmic agent to avoid inadvertent drug toxicity. Amiodarone and dofetilide are preferred in view of their favorable cardiac safety profile.61– 63 A randomized, double-blind, placebo-controlled trial conducted by Singh et al11 showed that amiodarone was significantly more effective in suppressing PVCs with concomitant improvement in LVEF in patients with congestive heart failure and asymptomatic ventricular arrhythmia. Downloaded from http://circep.ahajournals.org/ by guest on November 20, 2016 Catheter Ablation Catheter-based ablative approaches represent an emerging effective and alternative therapy to pharmacological treatment and have been increasingly reported over the past decade. Many studies have documented the improvement in LV function after catheter ablation of frequent PVCs (Table).10 –12,14,16,18,21,54 Yarlagadda et al12 noted a significant improvement in LVEF to near 60% in all patients with LV dysfunction who underwent successful catheter ablation of their frequent PVCs. Bogun et al15 documented the normalization of LVEF in 82% of patients who underwent catheter ablation for frequent PVCs and LV systolic dysfunction. Improvement of LVEF was also documented by Sarrazin et al10 after catheter ablation of frequent PVCs in the setting of prior myocardial infarction. Other studies also found significant reduction in LV end-diastolic dimensions of between 2 and 8 mm, mitral regurgitation by 75%, and New York Heart Association functional class by nearly 1 class.14,15,21 Wijnmaalen et al54 described a significant improvement in radial, circumferential, and longitudinal strain after catheter ablation in patients with frequent PVCs and preserved LVEF. However, like with any invasive intervention, the risks of catheter ablation (whether endocardial or epicardial) must be balanced against any potential benefits.56 Major complications occur in approximately 3% of cases, including death, stroke, myocardial infarction, atrioventricular block necessitating permanent pacemaker placement, cardiac perforation with or without pericardial tamponade, pericardial effusion, and blood vessel dissection or stenosis.64 Nevertheless, catheter ablation for PVCs is associated with a high success rate and few complications.12,14,15,21,58 Advancements and innovations in catheter ablation technology have favorably altered the efficacy–safety profile of ablation therapy. Our ability to predict the site of origin of the PVCs on surface electrocardiography65 and to safely access the right ventricular outflow tract and left ventricle (including the pericardium and the aortic cusp region)66,67 and the use of advanced 3-dimensional mapping tools allows us to precisely localize the PVC foci. Short-term ablation success rates of between 70% and 90% have been reported10,21,22,54; however, the long-term ablative outcomes remain to be studied. Alternative energy sources such as cryoablation may help improve the efficacy–safety profile as compared with traditional radiofrequency-based techniques.68 Given the favorable efficacy–safety profile of current catheter ablation techniques, we believe that catheter ablation is an increasingly appealing therapy for management of patients with suspected PVC- Premature Ventricular Contractions 233 induced cardiomyopathy. However, randomized clinical trials are needed to determine a comparative efficacy and outcome of modern medical against ablative approaches for those with frequent PVCs that are likely to be the cause of cardiomyopathy. Future Perspectives Knowledge of the molecular, cellular, and hemodynamic mechanisms of LV dysfunction in PVC-induced cardiomyopathy is limited. Despite the limited comparability between animal models and human subjects, animal models enable us to study the effects of PVCs and to understand the pathogenesis of PVC-induced cardiomyopathy. Development of better imaging techniques such as 2-dimensional speckle tracking strain imaging and cardiac MRI aimed at assessing early LV dysfunction and excluding occult structural heart disease allows the possibility of earlier detection of the disease. There is at present little evidence to recommend the routine use of such imaging techniques in the workup of PVC-induced cardiomyopathy. Although the suppression of PVCs is indicated for symptomatic patients with frequent PVCs and those with overt LV dysfunction, there is at present no evidence for the treatment of asymptomatic patients with normal LVEF to prevent PVC-induced cardiomyopathy. Further research is needed to identify the risk predictors for developing PVCinduced cardiomyopathy and to make a recommendation on the need and frequency of echocardiographic follow-up in this group of patients. In patients with a diagnosis of nonischemic cardiomyopathy and frequent PVCs with uncertainty as to the former being the cause or consequence of the latter, the plausibility of suppressing PVCs with medical or interventional therapy before placement of an implantable cardioverter– defibrillator (if current guidelines for its insertion are met) requires further study, bearing in mind that the cardiomyopathy is potentially reversible. In patients with decreased LVEF, a follow-up period of 3 to 12 months after initiation of antiarrhythmic therapy or catheter ablation is suggested to allow for recovery of LV function and to avoid unnecessary implantable cardioverter– defibrillator insertions in a potentially reversible condition.11,14,15,18 Where reduced LVEF persists despite diminished PVC burden, the decision as to the need for implantable cardioverter– defibrillator insertion should be governed by current guidelines.69 Frequent PVCs might be a factor responsible for the lack of response to medical therapy or cardiac resynchronization therapy. Suppression or elimination of PVCs may improve response to cardiac resynchronization therapy. Conclusions PVCs are a common occurrence within the general population. In the absence of structural heart disease, they typically carry a good prognosis. However, they may present with debilitating symptoms. PVCs have been implicated in the development of LV dysfunction and cardiomyopathy, but the risk factors and pathogenic mechanisms are incompletely understood. The suppression of PVCs using either antiarrhythmic pharmacological agents or emerging catheter ablation techniques appears to reverse the LV dysfunction. 234 Circ Arrhythm Electrophysiol February 2012 Table. Effects of Catheter Ablation of PVCs on Cardiac Function Downloaded from http://circep.ahajournals.org/ by guest on November 20, 2016 Study, Year Sample Size Inclusion Criteria Study Targets Effect of Intervention Outcome Yarlagadda et al,12 2005 27 (8 with depressed LVEF ⱕ45%) Frequent PVCs of LBBB and inferior axis morphology (mean of 17 624 PVCs over 24 h on Holter monitoring) Successful ablation (PVCs abolished during ablation and remained absent for ⱖ30 min in baseline state and during infusion of isoproterenol) Successful ablation in 23 patients, including 7 of 8 patients with low LVEF, reduction in PVCs from 17 541⫾11 479 to 507⫾722 (P⫽0.028) Significant improvement after ablation in LVEF in the 7 patients with depressed LVEF; mean LVEF increased from 39%⫾6% at baseline to 62%⫾6% (P⫽0.017) Sekiguchi et al,21 2005 47 ⬎10 000 PVCs per d Reduction in PVCs to ⬍1000 per d Successful ablation in 38 patients, reduction in PVCs from 23 989⫾13 366 to 137⫾249 (P⬍0.0001) After ablation, mean LVEDD decreased from 50⫾5 mm to 48⫾5 mm (P⬍0.01); mean LVESD decreased from 33⫾7 mm to 30⫾6 mm (P⬍0.01) Takemoto et al,14 2005 40 (14 with PVC burden ⬍10%; 12, 10%–20%; 14⬎20%) PVCs of LBBB and inferior axis morphology Successful ablation (noninducibility of PVCs with or without isoproterenol and/or programmed electrical stimulation for ⱖ30 min, nonrecurrence of PVCs for 72 h) Successful ablation in 37 patients, reduction in PVC burden in the ⬎20% group from 34%⫾3% to 1.3%⫾0.9% (P⬍0.01) Significant improvement for patients with PVC burden ⬎20%; LVEDD decreased from 54⫾1 mm to 47⫾1 mm, LVEF increased from 66%⫾2% to 72%⫾2%, MR decreased from 1.2°⫾0.2° to 0.3°⫾0.1° and NYHA functional class decreased from 1.8⫾0.2 to 1.0⫾0.0 (P⬍0.05 for all) Bogun et al,15 2007 60 (22 with depressed LVEF ⱕ50%) ⬎10 PVCs of various morphologies per hour over 24 h on Holter monitoring Successful ablation (PVCs abolished during ablation and uninducible by isoproterenol) Successful ablation in 48 patients, including 18 of 22 patients with depressed LVEF Significant improvement after ablation in the 18 patients with depressed LVEF; LVEF increased from 34%⫾13% to 59%⫾7% (P⬍0.001), LVEDD decreased from 59⫾6 mm to 51⫾8 mm (P⫽0.001), LVESD decreased from 45⫾7 mm to 34⫾7 mm (P⫽0.0002) Taieb et al,16 2007 6 Frequent PVCs of various morphologies and LV dysfunction (mean of 17 717 PVCs over 24 h on Holter monitoring) Successful ablation Successful ablation in all patients, reduction in PVCs from 17 717⫾7100 to 268⫾366 (P⫽0.006) LVEF increased from 42%⫾2.5% at baseline to 57%⫾3% (P⫽0.0001), mean LVEDD decreased from 60.0⫾3.5 mm to 54.0⫾3.7 mm (P⫽0.0009) Sarrazin et al,10 2009 30 (15 referred for ablation, 15 served as control) PVC burden of ⬎5% in patients with prior myocardial infarction Successful ablation Successful ablation in all 15 patients, reduction in PVC burden from 22%⫾12% to 2.6%⫾5.0% Significant improvement after ablation in LVEF; mean LVEF increased from 38%⫾11% to 51%⫾9% (P⬍0.0001); no improvement in LVEF was noted in the control group Baman et al,18 2010 174 (57 with depressed LVEF 35%⫾9%) Frequent PVCs of various morphologies (mean burden of 20%⫾16% on Holter monitoring) Successful ablation (80% reduction in PVC burden) Successful ablation in 146 patients, including 46 of 57 patients with depressed LVEF, reduction in PVC burden from 33%⫾14% to 1.9%⫾4.4% (P⬍0.01) Significant improvement in the 57 patients with depressed LVEF; LVEF increased from 35%⫾9% at baseline to 54%⫾10% (P⬍0.01), LVEDD decreased from 59⫾7 mm to 54⫾7 mm (P⬍0.01), LVESD decreased from 44⫾7 mm to 39⫾8 mm (P⬍0.01) 49 PVC burden of ⬎5% of various morphologies with normal LVEF, LV volumes, and RV dimensions Successful ablation (PVCs abolished during ablation and uninducible by isoproterenol) Successful ablation in 34 patients, reduction in PVC burden from 26%⫾13% to 0.2%⫾0.8% LV radial strain increased from 31.1%⫾14.2% to 45.5%⫾16.3% (P⬍0.0001), LV circumferential strain increased from ⫺16.2%⫾3.9% to ⫺18.9%⫾4.2% (P⫽0.004), LV longitudinal strain increased from ⫺17.8%⫾2.9% to ⫺19.6%⫾2.0% (P⫽0.007), RV longitudinal strain increased from ⫺24.2%⫾7.4% to ⫺28.4%⫾6.0% (P⫽0.009) Wijnmaalen et al,54 2010 PVCs indicates premature ventricular contractions; LVEF, left ventricular ejection fraction; LBBB, left bundle branch block; LV, left ventricular; RV, right ventricular, LVEDD, left ventricular end-diastolic dimension; MR, mitral regurgitation; NYHA, New York Heart Association; LVESD, left ventricular end-systolic dimension. Cha et al Disclosures None. References Downloaded from http://circep.ahajournals.org/ by guest on November 20, 2016 1. Messineo FC. Ventricular ectopic activity: prevalence and risk. Am J Cardiol. 1989;64:53J–56J. 2. Kostis JB, McCrone K, Moreyra AE, Gotzoyannis S, Aglitz NM, Natarajan N, Kuo PT. Premature ventricular complexes in the absence of identifiable heart disease. Circulation. 1981;63:1351–1356. 3. Sheldon SH, Gard JJ, Asirvatham SJ. Premature ventricular contractions and non-sustained ventricular tachycardia: association with sudden cardiac death, risk stratification, and management strategies. Indian Pacing Electrophysiol J. 2010;10:357–371. 4. Gaita F, Giustetto C, Di Donna P, Richiardi E, Libero L, Brusin MC, Molinari G, Trevi G. Long-term follow-up of right ventricular monomorphic extrasystoles. J Am Coll Cardiol. 2001;38:364 –370. 5. Kennedy HL, Whitlock JA, Sprague MK, Kennedy LJ, Buckingham TA, Goldberg RJ. Long-term follow-up of asymptomatic healthy subjects with frequent and complex ventricular ectopy. N Engl J Med. 1985;312: 193–197. 6. Ng GA. Treating patients with ventricular ectopic beats. Heart. 2006;92: 1707–1712. 7. Southall DP, Johnston F, Shinebourne EA, Johnston PG. 24-hour electrocardiographic study of heart rate and rhythm patterns in population of healthy children. Br Heart J. 1981;45:281–291. 8. Camm AJ, Evans KE, Ward DE, Martin A. The rhythm of the heart in active elderly subjects. Am Heart J. 1980;99:598 – 603. 9. Duffee DF, Shen WK, Smith HC. Suppression of frequent premature ventricular contractions and improvement of left ventricular function in patients with presumed idiopathic dilated cardiomyopathy. Mayo Clin Proc. 1998;73:430 – 433. 10. Sarrazin JF, Labounty T, Kuhne M, Crawford T, Armstrong WF, Desjardins B, Good E, Jongnarangsin K, Chugh A, Oral H, Pelosi F, Morady F, Bogun F. Impact of radiofrequency ablation of frequent post-infarction premature ventricular complexes on left ventricular ejection fraction. Heart Rhythm. 2009;6:1543–1549. 11. Singh SN, Fletcher RD, Fisher SG, Singh BN, Lewis HD, Deedwania PC, Massie BM, Colling C, Lazzeri D. Amiodarone in patients with congestive heart failure and asymptomatic ventricular arrhythmia. Survival Trial of Antiarrhythmic Therapy in Congestive Heart Failure. N Engl J Med. 1995;333:77– 82. 12. Yarlagadda RK, Iwai S, Stein KM, Markowitz SM, Shah BK, Cheung JW, Tan V, Lerman BB, Mittal S. Reversal of cardiomyopathy in patients with repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract. Circulation. 2005;112:1092–1097. 13. Niwano S, Wakisaka Y, Niwano H, Fukaya H, Kurokawa S, Kiryu M, Hatakeyama Y, Izumi T. Prognostic significance of frequent premature ventricular contractions originating from the ventricular outflow tract in patients with normal left ventricular function. Heart. 2009;95: 1230 –1237. 14. Takemoto M, Yoshimura H, Ohba Y, Matsumoto Y, Yamamoto U, Mohri M, Yamamoto H, Origuchi H. Radiofrequency catheter ablation of premature ventricular complexes from right ventricular outflow tract improves left ventricular dilation and clinical status in patients without structural heart disease. J Am Coll Cardiol. 2005;45:1259 –1265. 15. Bogun F, Crawford T, Reich S, Koelling TM, Armstrong W, Good E, Jongnarangsin K, Marine JE, Chugh A, Pelosi F, Oral H, Morady F. Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: comparison with a control group without intervention. Heart Rhythm. 2007;4:863– 867. 16. Taieb JM, Maury P, Shah D, Duparc A, Galinier M, Delay M, Morice R, Alfares A, Barnay C. Reversal of dilated cardiomyopathy by the elimination of frequent left or right premature ventricular contractions. J Interv Card Electrophysiol. 2007;20:9 –13. 17. Kanei Y, Friedman M, Ogawa N, Hanon S, Lam P, Schweitzer P. Frequent premature ventricular complexes originating from the right ventricular outflow tract are associated with left ventricular dysfunction. Ann Noninvasive Electrocardiol. 2008;13:81– 85. 18. Baman TS, Lange DC, Ilg KJ, Gupta SK, Liu TY, Alguire C, Armstrong W, Good E, Chugh A, Jongnarangsin K, Pelosi F Jr, Crawford T, Ebinger M, Oral H, Morady F, Bogun F. Relationship between burden of premature ventricular complexes and left ventricular function. Heart Rhythm. 2010;7:865– 869. Premature Ventricular Contractions 235 19. Hasdemir C, Ulucan C, Yavuzgil O, Yuksel A, Kartal Y, Simsek E, Musayev O, Kayikcioglu M, Payzin S, Kultursay H, Aydin M, Can LH. Tachycardia-induced cardiomyopathy in patients with idiopathic ventricular arrhythmias: the incidence, clinical and electrophysiologic characteristics, and the predictors. J Cardiovasc Electrophysiol. 2011;22: 663– 668. 20. Shanmugam N, Chua TP, Ward D. ‘Frequent’ ventricular bigeminy—a reversible cause of dilated cardiomyopathy. How frequent is ‘frequent’? Eur J Heart Fail. 2006;8:869 – 873. 21. Sekiguchi Y, Aonuma K, Yamauchi Y, Obayashi T, Niwa A, Hachiya H, Takahashi A, Nitta J, Iesaka Y, Isobe M. Chronic hemodynamic effects after radiofrequency catheter ablation of frequent monomorphic ventricular premature beats. J Cardiovasc Electrophysiol. 2005;16:1057–1063. 22. Del Carpio Munoz F, Syed FF, Noheria A, Cha YM, Friedman PA, Hammill SC, Munger TM, Venkatachalam KL, Shen WK, Packer DL, Asirvatham SJ. Characteristics of premature ventricular complexes as correlates of reduced left ventricular systolic function: study of the burden, duration, coupling interval, morphology and site of origin of PVCs. J Cardiovasc Electrophysiol. 2011;22:791–798. 23. Gami AS, Noheria A, Lachman N, Edwards WD, Friedman PA, Talreja D, Hammill SC, Munger TM, Packer DL, Asirvatham SJ. Anatomical correlates relevant to ablation above the semilunar valves for the cardiac electrophysiologist: a study of 603 hearts. J Interv Card Electrophysiol. 2011;30:5–15. 24. Steinberg JS, Fischer A, Wang P, Schuger C, Daubert J, McNitt S, Andrews M, Brown M, Hall WJ, Zareba W, Moss AJ. The clinical implications of cumulative right ventricular pacing in the multicenter automatic defibrillator trial II. J Cardiovasc Electrophysiol. 2005;16: 359 –365. 25. Blanc JJ, Fatemi M, Bertault V, Baraket F, Etienne Y. Evaluation of left bundle branch block as a reversible cause of non-ischaemic dilated cardiomyopathy with severe heart failure. A new concept of left ventricular dyssynchrony-induced cardiomyopathy. Europace. 2005;7:604 – 610. 26. Gardiwal A, Yu H, Oswald H, Luesebrink U, Ludwig A, Pichlmaier AM, Drexler H, Klein G. Right ventricular pacing is an independent predictor for ventricular tachycardia/ventricular fibrillation occurrence and heart failure events in patients with an implantable cardioverter– defibrillator. Europace. 2008;10:358 –363. 27. Lee SJ, McCulloch C, Mangat I, Foster E, De Marco T, Saxon LA. Isolated bundle branch block and left ventricular dysfunction. J Card Fail. 2003;9:87–92. 28. Spragg DD, Kass DA. Pathobiology of left ventricular dyssynchrony and resynchronization. Prog Cardiovasc Dis. 2006;49:26 – 41. 29. Tantengco MV, Thomas RL, Karpawich PP. Left ventricular dysfunction after long-term right ventricular apical pacing in the young. J Am Coll Cardiol. 2001;37:2093–2100. 30. Moulton KP, Medcalf T, Lazzara R. Premature ventricular complex morphology. A marker for left ventricular structure and function. Circulation. 1990;81:1245–1251. 31. Sun Y, Blom NA, Yu Y, Ma P, Wang Y, Han X, Swenne CA, van der Wall EE. The influence of premature ventricular contractions on left ventricular function in asymptomatic children without structural heart disease: an echocardiographic evaluation. Int J Cardiovasc Imaging. 2003;19:295–299. 32. Olgun H, Yokokawa M, Baman T, Kim HM, Armstrong W, Good E, Chugh A, Pelosi F Jr, Crawford T, Oral H, Morady F, Bogun F. The role of interpolation in PVC-induced cardiomyopathy. Heart Rhythm. 2011; 8:1046 –1049. 33. Otsuji Y, Toda H, Kisanuki A, Koyano T, Kuroiwa R, Murayama T, Matsushita R, Nakao S, Tomari T, Tanaka H. Influence of left ventricular filling profile during preceding control beats on pulse pressure during ventricular premature contractions. Eur Heart J. 1994;15:462– 467. 34. Lerman BB, Belardinelli L, West GA, Berne RM, DiMarco JP. Adenosine-sensitive ventricular tachycardia: evidence suggesting cyclic AMPmediated triggered activity. Circulation. 1986;74:270 –280. 35. Cooper MW. Postextrasystolic potentiation. Do we really know what it means and how to use it? Circulation. 1993;88:2962–2971. 36. Wichterle D, Melenovsky V, Simek J, Malik J, Malik M. Hemodynamics and autonomic control of heart rate turbulence. J Cardiovasc Electrophysiol. 2006;17:286 –291. 37. Segerson NM, Wasmund SL, Abedin M, Pai RK, Daccarett M, Akoum N, Wall TS, Klein RC, Freedman RA, Hamdan MH. Heart rate turbulence parameters correlate with post-premature ventricular contraction changes in muscle sympathetic activity. Heart Rhythm. 2007;4:284 –289. 236 Circ Arrhythm Electrophysiol February 2012 Downloaded from http://circep.ahajournals.org/ by guest on November 20, 2016 38. Takada H, Takeuchi S, Ando K, Kaito A, Yoshida S. Experimental studies on myocardial contractility and hemodynamics in extrasystoles. Jpn Circ J. 1970;34:419 – 430. 39. Kass DA. Pathophysiology of physiologic cardiac pacing: advantages of leaving well enough alone. JAMA. 2002;288:3159 –3161. 40. Goldberger JJ, Kadish AH. Cardiac memory. Pacing Clin Electrophysiol. 1999;22:1672–1679. 41. Adomian GE, Beazell J. Myofibrillar disarray produced in normal hearts by chronic electrical pacing. Am Heart J. 1986;112:79 – 83. 42. Lee MA, Dae MW, Langberg JJ, Griffin JC, Chin MC, Finkbeiner WE, O’Connell JW, Botvinick E, Scheinman MM, Rosenqvist M. Effects of long-term right ventricular apical pacing on left ventricular perfusion, innervation, function and histology. J Am Coll Cardiol. 1994;24: 225–232. 43. van Oosterhout MF, Prinzen FW, Arts T, Schreuder JJ, Vanagt WY, Cleutjens JP, Reneman RS. Asynchronous electrical activation induces asymmetrical hypertrophy of the left ventricular wall. Circulation. 1998; 98:588 –595. 44. Akoum NW, Daccarett M, Wasmund SL, Hamdan MH. An animal model for ectopy-induced cardiomyopathy. Pacing Clin Electrophysiol. 2011; 34:291–295. 45. Huizar JF, Kaszala K, Potfay J, Minisi AJ, Lesnefsky EJ, Abbate A, Mezzaroma E, Chen Q, Kukreja RC, Hoke NN, Thacker LR II, Ellenbogen KA, Wood MA. Left ventricular systolic dysfunction induced by ventricular ectopy: a novel model for premature ventricular contraction-induced cardiomyopathy. Circ Arrhythm Electrophysiol. 2011;4:543–549. 46. Smith ML, Hamdan MH, Wasmund SL, Kneip CF, Joglar JA, Page RL. High-frequency ventricular ectopy can increase sympathetic neural activity in humans. Heart Rhythm. 2010;7:497–503. 47. Wilber DJ. Ventricular ectopic beats: not so benign. Heart. 2009;95: 1209 –1210. 48. Tikkanen JT, Anttonen O, Junttila MJ, Aro AL, Kerola T, Rissanen HA, Reunanen A, Huikuri HV. Long-term outcome associated with early repolarization on electrocardiography. N Engl J Med. 2009;361: 2529 –2537. 49. Bhushan M, Asirvatham SJ. The conundrum of ventricular arrhythmia and cardiomyopathy: which abnormality came first? Curr Heart Fail Rep. 2009;6:7–13. 50. Delgado V, Ypenburg C, van Bommel RJ, Tops LF, Mollema SA, Marsan NA, Bleeker GB, Schalij MJ, Bax JJ. Assessment of left ventricular dyssynchrony by speckle tracking strain imaging comparison between longitudinal, circumferential, and radial strain in cardiac resynchronization therapy. J Am Coll Cardiol. 2008;51:1944 –1952. 51. Edvardsen T, Helle-Valle T, Smiseth OA. Systolic dysfunction in heart failure with normal ejection fraction: speckle-tracking echocardiography. Prog Cardiovasc Dis. 2006;49:207–214. 52. Leitman M, Lysyansky P, Sidenko S, Shir V, Peleg E, Binenbaum M, Kaluski E, Krakover R, Vered Z. Two-dimensional strain-a novel software for real-time quantitative echocardiographic assessment of myocardial function. J Am Soc Echocardiogr. 2004;17:1021–1029. 53. Reisner SA, Lysyansky P, Agmon Y, Mutlak D, Lessick J, Friedman Z. Global longitudinal strain: a novel index of left ventricular systolic function. J Am Soc Echocardiogr. 2004;17:630 – 633. 54. Wijnmaalen AP, Delgado V, Schalij MJ, van Huls van Taxis CF, Holman ER, Bax JJ, Zeppenfeld K. Beneficial effects of catheter ablation on left ventricular and right ventricular function in patients with frequent premature ventricular contractions and preserved ejection fraction. Heart. 2010;96:1275–1280. 55. Abdalla IS, Prineas RJ, Neaton JD, Jacobs DR Jr, Crow RS. Relation between ventricular premature complexes and sudden cardiac death in apparently healthy men. Am J Cardiol. 1987;60:1036 –1042. 56. Ezzat VA, Liew R, Ward DE. Catheter ablation of premature ventricular contraction-induced cardiomyopathy. Nat Clin Pract Cardiovasc Med. 2008;5:289 –293. 57. Krittayaphong R, Bhuripanyo K, Punlee K, Kangkagate C, Chaithiraphan S. Effect of atenolol on symptomatic ventricular arrhythmia without structural heart disease: a randomized placebo-controlled study. Am Heart J. 2002;144:e10. 58. Zhu DW, Maloney JD, Simmons TW, Nitta J, Fitzgerald DM, Trohman RG, Khoury DS, Saliba W, Belco KM, Rizo-Patron C, Pinski SL. Radiofrequency catheter ablation for management of symptomatic ventricular ectopic activity. J Am Coll Cardiol. 1995;26:843– 849. 59. Capucci A, Di Pasquale G, Boriani G, Carini G, Balducelli M, Frabetti L, Carozzi A, Finzi A, Pinelli G, Magnani B. A double-blind crossover comparison of flecainide and slow-release mexiletine in the treatment of stable premature ventricular complexes. Int J Clin Pharmacol Res. 1991; 11:23–33. 60. Echt DS, Liebson PR, Mitchell LB, Peters RW, Obias-Manno D, Barker AH, Arensberg D, Baker A, Friedman L, Greene HL, Huther ML, Richardson DW. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. N Engl J Med. 1991;324:781–788. 61. Effect of prophylactic amiodarone on mortality after acute myocardial infarction and in congestive heart failure: meta-analysis of individual data from 6500 patients in randomised trials. Amiodarone Trials Meta-Analysis Investigators. Lancet. 1997;350:1417–1424. 62. Vorperian VR, Havighurst TC, Miller S, January CT. Adverse effects of low dose amiodarone: a meta-analysis. J Am Coll Cardiol. 1997;30: 791–798. 63. Torp-Pedersen C, Moller M, Bloch-Thomsen PE, Kober L, Sandoe E, Egstrup K, Agner E, Carlsen J, Videbaek J, Marchant B, Camm AJ. Dofetilide in patients with congestive heart failure and left ventricular dysfunction. Danish Investigations of Arrhythmia and Mortality on Dofetilide Study Group. N Engl J Med. 1999;341:857– 865. 64. Wellens HJ. Catheter ablation of cardiac arrhythmias: usually cure, but complications may occur. Circulation. 1999;99:195–197. 65. Dixit S, Gerstenfeld EP, Callans DJ, Marchlinski FE. Electrocardiographic patterns of superior right ventricular outflow tract tachycardias: distinguishing septal and free-wall sites of origin. J Cardiovasc Electrophysiol. 2003;14:1–7. 66. Daniels DV, Lu YY, Morton JB, Santucci PA, Akar JG, Green A, Wilber DJ. Idiopathic epicardial left ventricular tachycardia originating remote from the sinus of Valsalva: electrophysiological characteristics, catheter ablation, and identification from the 12-lead electrocardiogram. Circulation. 2006;113:1659 –1666. 67. Ouyang F, Fotuhi P, Ho SY, Hebe J, Volkmer M, Goya M, Burns M, Antz M, Ernst S, Cappato R, Kuck KH. Repetitive monomorphic ventricular tachycardia originating from the aortic sinus cusp: electrocardiographic characterization for guiding catheter ablation. J Am Coll Cardiol. 2002; 39:500 –508. 68. Kurzidim K, Schneider HJ, Kuniss M, Sperzel J, Greiss H, Berkowitsch A, Pitschner HF. Cryocatheter ablation of right ventricular outflow tract tachycardia. J Cardiovasc Electrophysiol. 2005;16:366 –369. 69. Epstein AE, DiMarco JP, Ellenbogen KA, Estes NA III, Freedman RA, Gettes LS, Gillinov AM, Gregoratos G, Hammill SC, Hayes DL, Hlatky MA, Newby LK, Page RL, Schoenfeld MH, Silka MJ, Stevenson LW, Sweeney MO, Smith SC Jr, Jacobs AK, Adams CD, Anderson JL, Buller CE, Creager MA, Ettinger SM, Faxon DP, Halperin JL, Hiratzka LF, Hunt SA, Krumholz HM, Kushner FG, Lytle BW, Nishimura RA, Ornato JP, Riegel B, Tarkington LG, Yancy CW. ACC/AHA/HRS 2008 Guidelines for Device-Based Therapy of Cardiac Rhythm Abnormalities: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines (Writing Committee to Revise the ACC/AHA/NASPE 2002 Guideline Update for Implantation of Cardiac Pacemakers and Antiarrhythmia Devices): developed in collaboration with the American Association for Thoracic Surgery and Society of Thoracic Surgeons. Circulation. 2008;117:e350 – 408. KEY WORDS: arrhythmia 䡲 cardiomyopathy 䡲 heart failure ventricular contractions 䡲 ventricular arrhythmia 䡲 premature Premature Ventricular Contraction-Induced Cardiomyopathy: A Treatable Condition Yong-Mei Cha, Glenn K. Lee, Kyle W. Klarich and Martha Grogan Downloaded from http://circep.ahajournals.org/ by guest on November 20, 2016 Circ Arrhythm Electrophysiol. 2012;5:229-236 doi: 10.1161/CIRCEP.111.963348 Circulation: Arrhythmia and Electrophysiology is published by the American Heart Association, 7272 Greenville Avenue, Dallas, TX 75231 Copyright © 2012 American Heart Association, Inc. All rights reserved. Print ISSN: 1941-3149. Online ISSN: 1941-3084 The online version of this article, along with updated information and services, is located on the World Wide Web at: http://circep.ahajournals.org/content/5/1/229 An erratum has been published regarding this article. Please see the attached page for: /content/5/2/e62.full.pdf Permissions: Requests for permissions to reproduce figures, tables, or portions of articles originally published in Circulation: Arrhythmia and Electrophysiology can be obtained via RightsLink, a service of the Copyright Clearance Center, not the Editorial Office. Once the online version of the published article for which permission is being requested is located, click Request Permissions in the middle column of the Web page under Services. Further information about this process is available in the Permissions and Rights Question and Answer document. Reprints: Information about reprints can be found online at: http://www.lww.com/reprints Subscriptions: Information about subscribing to Circulation: Arrhythmia and Electrophysiology is online at: http://circep.ahajournals.org//subscriptions/ Correction In the article, “Premature Ventricular Contraction-Induced Cardiomyopathy: A Treatable Condition,” by Cha et al, which appeared in the February 2012 issue of the journal (Circ Arrhythm Electrophysiol. 2012;5:229 –236), the order of authors is incorrect. The correct order is as follows: Glenn K. Lee, MBBS; Kyle W. Klarich, MD; Martha Grogan, MD; Yong-Mei Cha, MD The online version of the article has been corrected. The authors regret the error. Reference 1. Cha Y-M, Lee GK, Klarich KW, Grogan M. Premature ventricular contraction-induced cardiomyopathy: a treatable condition. Circ Arrhythm Electrophysiol. 2012;5:229 —236. (Circ Arrhythm Electrophysiol. 2012;5:e62.) © 2012 American Heart Association, Inc. Circ Arrhythm Electrophysiol is available at http://circep.ahajournals.org e62 DOI: 10.1161/HAE.0b013e3182564842