The PVC and Cardiomyopathy: Which Came First?

Linda Moulton, RN, MS Owner, Critical Care ED and C.C.E. Consulting Faculty, Order and Disorder Electrophysiology Training Program New Berlin, Illinois
Linda Moulton, RN, MS Owner, Critical Care ED and C.C.E. Consulting Faculty, Order and Disorder Electrophysiology Training Program New Berlin, Illinois

Premature ventricular contractions (PVCs) are found frequently in patients both with structural heart disease and without disease. The recommended treatment for PVCs has been evolving over the years. The level of importance relegated to the presence of PVCs has also been a moving target. Recent studies have brought the role of the PVC back into the spotlight, as PVCs are thought to be the cause of cardiomyopathies in some patients. This article will review past beliefs about the PVC, and discuss some new thoughts and approaches.

Early Thoughts

In 1957 Leo Schamroth stated that ‘ectopic beats, regardless of the type, may in themselves have no diagnostic or diagnostic significance’ … ‘…when associated with organic heart disease, as in myocardial infarction, they are significant, and may herald the approach of more serious ectopic rhythms such as ventricular tachycardia’1 (Figure 1). A version of his text in 1971 stated that in the absence of heart disease, PVC treatment was not required. However, if the presence of the arrhythmia induced anxiety, small doses of beta blockers might be helpful. If the PVCs were associated with myocardial infarction (MI), had a short coupling interval, were associated with repetitive paroxysmal tachycardia, occurred in pairs, were associated with digitalis intoxication, or were bigeminal or multiform, treatment was warranted.2 In the 1982 edition of Schamroth’s An Introduction to Electrocardiography,3 the importance of the presence of PVCs was stated in the following: ‘Unifocal ventricular extrasystoles are usually indicative of cardiac disease if (a) they occur frequently…, (b) they occur in bigeminal rhythm, (c) they occur in association with cardiac disease, (d) they occur in persons over 40 years of age or (e) they are precipitated by exercise.’ The attempt to define which PVC situation warranted treatment was very much an ongoing task, and the parameters for treatment were continually being tweaked. The interaction of PVCs and cardiomyopathy was not discussed in these earlier texts. The reports in the literature about an interaction started appearing in research conducted in the 1980s. The first discussion is of the presence of PVCs in the setting of MI.

PVCs Post Myocardial Infarction

The role of MI and ventricular remodeling in increasing the incidence of PVCs was documented in the 1980s. A representative study is that conducted by Mukharji et al,4 who followed 533 patients who had survived MI for up to 24 months. The investigators found that the presence of frequent PVCs in the setting of LV dysfunction early post MI predicted high risk for sudden cardiac death over the subsequent seven months. In another study, Bigger et al5 followed 766 post-MI patients from nine hospitals, looking at PVC frequency, left ventricular function, and mortality. They found that left ventricular ejection fraction (LVEF) below 30% was a better predictor of early mortality (less than six months) and that frequency of ventricular arrhythmias was a better predictor of late mortality (after six months). Based on the data from these and multiple other studies, the Cardiac Arrhythmia Suppression Trial (CAST) was conducted.

The PVC Hypothesis, the CAST Trial, and Current Guidelines

The PVC hypothesis was a belief that the suppression of ventricular arrhythmias with antiarrhythmic drugs would impact survival for the post-MI patient. Clinical studies such as the CAST6-8 were conducted in the late 1980s and early 1990s to test that hypothesis. The post-MI patients who had impaired left ventricular function and participated in these trials experienced either harmful effects or no positive impact on survival. In the CAST I study and SWORD, there was actually increased all-cause mortality and increased mortality, respectively, in the groups receiving the antiarrhythmic agents.6,8  These results had the effect of throwing cold water on the idea of primary prevention of PVCs with antiarrhythmics. The only category of antiarrhythmic that had been shown to consistently improve survival while decreasing arrhythmic mortality has been the beta blockers.9-11

As a result of these studies, two directions for management of PVCs became more clarified: management in the absence of structural heart disease and management in the presence of structural heart disease. For those without structural disease, ventricular ectopy was thought to have no significance prognostically. Antiarrhythmic agents were believed not to be indicated unless symptoms were present; then treatment with beta blockers or IC agents were preferred.12-13 The approach for patients with structural heart disease, as demonstrated by reduced LVEF, has been guided by the results from trials such as AVID, MADIT, MUSST, MADIT II, DEFINITE, and SCD-HeFT, which formed the basis for our current ICD and cardiac resynchronization guidelines.15-19

More Studies

Some studies began to look at changes that occurred with PVCs and cardiomyopathy over time in the post-MI population and in the heart failure population. Pfeffer and Braunwald20 reported that the ventricular remodeling after MI involved progressive dilation, hypertrophy, altered cavity shape, and a decrease in contractile function. St John et al21 found a relationship between left ventricular remodeling and ventricular arrhythmias post myocardial infarction in the Survival and Ventricular Enlargement (SAVE) trial. Patients were followed for over two years to determine changes in the echocardiogram and the Holter monitor PVCs frequency. Investigators reported that altered LV architecture and function during remodeling provided a substrate capable of triggering ventricular arrhythmias.

The PROMISE study (Prospective Randomized Milrinone Survival Evaluation)22 looked at 1,080 heart failure patients (class III/IV). The study results suggested that asymptomatic ventricular arrhythmias did not specifically predict sudden death in those with moderate-to-severe heart failure.

Moulton23 reported that a broadly notched PVC of long duration (≥160 msec) was a reliable marker for a dilated and globally hypokinetic left ventricle and that PVCs with a smooth contour or narrow notching, and a short duration reflected a normal heart size and normal or near-normal systolic function.

PVCs and Left Ventricular Function

The years that followed have been filled with a variety of studies which sought to capture the relevance of the PVC to those without structural heart disease. Hemodynamic and echocardiographic parameters were collected, as were data about PVC burden. The type of PVC or tachycardia more likely to lead to cardiomyopathy was explored. Much of the work looked at the population with right ventricular outflow tract (RVOT) PVCs/tachycardia. The following is a brief summary of some of these studies that tried to determine which really came first, the ventricular arrhythmia or the cardiomyopathy.

A 1997 case report24 of a patient with dilated cardiomyopathy and repetitive nonsustained monomorphic ventricular tachycardia disclosed that radiofrequency catheter ablation (RFCA) of an RVOT tachycardia led to improvement in LV systolic function and resolution of heart failure symptoms. This is seemingly one of the first reports of ablation of a ventricular ectopic focus reversing heart failure. Chugh et al25 in 2000 also reported the resolution of a dilated cardiomyopathy after ablation of a focal PVC source. The authors suggested that this approach is a way to decrease the prevalence of some dilated cardiomyopathies.

The chronic hemodynamic effects of the PVC were evaluated in a study by Sekiguchi et al.26 They studied patients with frequent PVCs (greater than 10,000 per day) who had no underlying heart disease and who underwent RFCA. These patients were evaluated prior to ablation with echocardiographic testing and serum B-type natriuretic peptide (BNP) levels, and followed with repeat measurements. Nine patients were treated unsuccessfully. Left ventricular dimensions and serum BNP levels improved significantly for those with successful ablations and did not for those with unsuccessful ablations or recurrences. 

A number of studies have examined patients with RVOT PVCs and tachycardias (Figure 2). Yarlagadda et al27 studied 27 patients with repetitive monomorphic ventricular ectopy originating from the RVOT. Successful ablation was performed in 23. Seven of the eight with depressed LV function experienced improved function post ablation. Another study from 200528 studied 40 patients with RVOT ectopic beats. They collected data on PVC frequency, LVEF, LV diastolic dimension (LVDd), mitral valve function by echocardiogram, cardiothoracic ratio by chest x-ray, and NYHA functional class information. Patients were evaluated before and 6–12 months after RFCA. For those with >20% PVCs, all parameters improved (p < 0.05) compared with before. For those with <20% PVC on pre ablation, a significant difference was seen between groups in all parameters. The authors stated that RFCA produced definite clinical benefits. The ACC/AHA/ESC 2006 Guidelines for Management of Patients with Ventricular Arrhythmias reflected the results of many of these studies when it stated that when PVCs are frequent, ablation of asymptomatic PVCs can be considered to avoid the tachycardia-induced cardiomyopathy. This is a Class IIb indication.29

In 2007 Bogun et al30 reported on their study of 60 patients with idiopathic PVCs greater than 10/hour. They found a decreased LVEF in 37%. Those with decreased LVEFs tended to have greater PVC burdens. Thirty-one had RVOT sites of origin, nine had LVOT sites, and 13 had sites in other locations. Successful ablation was achieved in 48 (80%). Of those with abnormal LVEFs before ablation, the left ventricles normalized in 82% within six months. The four with ineffective ablations experienced a further LVEF decline. A control group with decreased LVEFs, a similar PVC burden and no ablation had unchanged LVEFs over the follow-up time; one had a heart transplant.

Niwano et al31 studied 239 patients with PVCs (>1,000/day). All sites of origin were either the right or left ventricular outflow tracts, and no patients had heart disease. The cohort was followed for at least four years. No serious events were recorded. There were no LVEF or mean LVDd changes that were considered significant. A negative correlation was found between the PVC prevalence and DeltaLVEF, and a positive correlation between PVC prevalence and DeltaLVDd. Thirteen patients had LV dysfunction defined by DeltaLVEF ≥6%. The authors suggested that paying attention over the long term to the possible progression of LV dysfunction in this population was an important consideration. In a 2010 study,32 an attempt was made to determine a cutoff PVC burden that can result in PVC-induced cardiomyopathy. A total of 174 consecutive patients were referred for idiopathic PVC ablation. Forty-two of 174 had NSVT. The PVC burden was assessed. A reduced LVEF was found in 33%; these patients had a mean PVC burden of 33%. The authors found that a PVC burden >24% seemed to separate populations. The lowest PVC burden with reversibility of cardiomyopathy post ablation was 10%.

Two studies looked at the role of parasystolic PVCs and interpolated PVCs. PVCs from the left ventricular septum (not fascicular sites) were the focus of a study by Jia et al33 in 2011. This study included 20 patients who were symptomatic. Pace mapping and activation mapping were conducted during ablation. There was a 70% incidence of ventricular parasystole present. Ventricular tachycardia was not inducible by stimulation or isoproterenol, and Purkinje potentials were not present at the site of ablation. The results suggested this was a myocardial, not a fascicular, substrate. Another study in 2011 assessed the role of PVC interpolation in PVC-induced cardiomyopathy.34 Fifty-one consecutive patients were studied. The LVEF mean was 49. Holter monitor results were used to determine the amount of interpolation. Electrophysiologic studies were performed using programmed stimulation to r/o ventricular tachycardia with and without isoproterenol. Mapping and ablation were carried out and considered effective if there was an ≥80% reduction in PVC burden achieved. PVC-induced cardiomyopathy was defined as an abnormal LVEF that improved at least 15% or normalized after ablation. Of those with cardiomyopathies, 14 of 21 had interpolated PVCs. Only six of 30 without cardiomyopathy had interpolated PVCs. Those with interpolated PVCs had a higher PVC burden. During electrophysiologic studies, the presence of ventriculoatrial block at a ventricular pacing cycle length of 600 ms correlated with the presence of interpolation (p = .004). Patients with interpolation had a longer mean ventriculoatrial block cycle length than those without interpolated PVCs (p = .01). The authors concluded that interpolation was predictive of cardiomyopathy above PVC burden alone.

The characteristics of PVCs that lead to cardiomyopathy and attempts at prediction were the subjects of the following studies in 2011 and 2012. Del Carpio et al35 listed the following as characteristics that may be associated with cardiomyopathy: PVC burden, longer PVC duration, presence of nonsustained VT, multiform PVCs, and right ventricular PVCs. Another study by Yokokawa et al36 found that broader PVCs and those that are epicardial in origin were associated with the development of reversible cardiomyopathy independent of the PVC burden. Yet another study sought to determine the electrocardiographic and electrophysiologic characteristics of PVC-mediated LV dysfunction.37 The study included 127 patients undergoing RFCA who had frequent PVCs (>10%/24 hours) and no significant structural disease. The LVEF was <50% in 28 of 127. For these 28, the likelihood of more PVCs, the presence of NSVT, and a retrograde p wave following the PVC was significantly greater. Left ventricular dysfunction was seen with a PVC burden at 26%/day. PVC morphology, axis, width, coupling interval, interpolation, and the presence of exercise-induced PVCs was not significantly different between the two groups. The most significant predictors of cardiomyopathy were PVC burden >26%/day and the presence of retrograde p waves.

These final two studies examined the efficacy of antiarrhythmic drugs and prediction of LVEF recovery. Stec et al38 evaluated the short- and long-term efficacy of antiarrhythmic drugs and RFCA in the setting of symptomatic PVCs and no organic heart disease. Propafenone was the drug seen as most efficacious, then verapamil, then metoprolol. Of those studied in this trial, 60% underwent RFCA, averaging 1.2 procedures per patient. Ablation was effective in 44/50 patients. Optimal benefit was seen with ablation. Patient symptoms were measured by use of a visual analogue scale. The second study39 involved 87 patients in whom the time course and predictors of recovery from left ventricular dysfunction after PVC ablation were measured. Ejection fraction normalized at a mean of five months post ablation. The majority of patients experienced LV function recovery in four months. The QRS width was significantly longer in those with delayed recovery. In about 33% of subjects, recovery was delayed and took up to 45 months.

Further Echocardiographic Assessment

A few studies have emerged over the last five years reporting the use of speckle tracking strain imaging to detect subtle changes in the ventricles. Speckle tracking strain imaging allows angle-independent evaluation of multidirectional LV strain in radial, circumferential and longitudinal directions, and RV longitudinal strain.40 This is a feature not available with standard echocardiographic testing. The problem of angle dependency is solved and two deformation components are estimated simultaneously.41-42 This technique has been used some in heart failure research.

Wijnmaalen et al43 incorporated speckle tracking into their study. The investigators studied patients with PVCs, many of whom had normal ejection fractions. The study sought to identify what effect PVCs had on LV function in patients with preserved LVEFs. There were 49 patients with PVCs and 25 healthy controls. Thirty-four patients with PVCs had ablations. Speckle tracking showed a reduced LV and RV strain in the PVC group compared with controls. However, follow up showed no changes in the treated and untreated in LVEF, LV volumes, and RV dimensions and function. Radial (RS), circumferential (CS) and longitudinal (LS) strain improved significantly after RFCA for the treatment group, but was unchanged in the untreated patients. Therefore, the findings of the conventional echocardiogram were not sensitive enough to detect these early changes.

Yao et al44 studied 30 patients with RVOT PVCs and no evidence of structural heart disease, and compared them to 30 healthy subjects. Aortic systolic velocity-time integral and myocardium strain in CS, RS and LS directions were evaluated by conventional echocardiography and speckle tracking image. For the PVC group, a significant difference in global CS, RS and LS, as well as in segmental RS and LS, was found in nearly all left ventricular segments. The authors suggested that speckle tracking imaging could be useful to detect changes in ventricular function in the PVC setting earlier than conventional echocardiogram.

Prediction of PVCs as the Initial Event

So how do we know which population will experience a reversal of cardiomyopathy when PVCs are ablated? Bhushan and Asirvatham have developed criteria for what they believe defines the situation in which PVCs precede cardiomyopathy.45 The authors believe this will help in identifying which patients will benefit from ablation or being placed on antiarrhythmic agents, and have a cardiomyopathy reversal. They have included the following: absence of underlying cardiac disease; absence of coronary artery disease; PVCs >20,000 per day; one or two primary PVC morphologies; origin in RVOT, LVOT, or fascicular; and preserved myocardial thickness and absence of scar on echocardiogram (Table 1).

RF ablation for frequent PVCs in patients without structural heart disease has been shown to completely reverse cardiomyopathy in numerous studies. Determining whether PVCs appeared first is challenging. Some clues are starting to emerge. Treatment of these patients with RFCA has been shown to be of tremendous benefit. 


  1. Schamroth L. An Introduction to Electrocardiography. Blackwell, Oxford, 1957, p. 48.
  2. Schamroth L. The Disorders of Cardiac Rhythm. Blackwell, Oxford, 1971.
  3. Schamroth L. An Introduction to Electrocardiography, Sixth Edition. Blackwell, Oxford, 1982. p. 187.
  4. Mukharji J, Rude RE, Poole WK, et al. Risk factors for sudden death after acute myocardial infarction: two-year follow-up. Am J Cardiol. 1984;54:31-36.
  5. Bigger JT, Fleiss JL, Kleiger R, et al. The relationships among ventricular arrhythmias, left ventricular dysfunction, and mortality in the 2 years after myocardial infarction. Circulation. 1984;69:250-258.
  6. Echt DS, Liebson PR, Mitchell LB, et al. Mortality and morbidity in patients receiving encainide, flecainide, or placebo. The Cardiac Arrhythmia Suppression Trial. N Engl J Med. 1991;324:781-788.
  7. The Cardiac Arrhythmia Suppression Trial II Investigators. Effect of the antiarrhythmic agent moricizine on survival after myocardial infarction. N Engl J Med. 1992;327:227-233.
  8. Waldo AL, Camm AJ, deRuyter H, et al. Effect of d-sotalol on mortality in patients with left ventricular dysfunction after recent and remote myocardial infarction. The SWORD Investigators. Survival With Oral d-Sotalol. Lancet. 1996;348:7-12.
  9. Waagstein F, Bristow MR, Swedberg K, et al. Beneficial effects of metoprolol in idiopathic dilated cardiomyopathy. Metoprolol in Dilated Cardiomyopathy (MDC) Trial Study Group. Lancet. 1993;342:1441-1446.
  10. Packer M, Bristow MR, Cohn JN, et al. The effect of carvedilol on morbidity and mortality in patients with chronic heart failure. U.S. Carvedilol Heart Failure Study Group. N Engl J Med. 1996;334:1349-1355.
  11. Dargie HJ. Effect of carvedilol on outcome after myocardial infarction in patients with left-ventricular dysfunction: the CAPRICORN randomized trial. Lancet. 2001;357:1385-1390.
  12. Conti CR. Ventricular arrhythmias: a general cardiologist’s assessment of therapies in 2005. Clin Cardiol. 2005;28:314-316.
  13. Gaita F, Giustetto C, Di Donna P, et al. Long-term follow-up of right ventricular monomorphic extrasystoles. J Am Coll Cardiol. 2001;38:364-370.
  14. The Antiarrhythmics versus Implantable Defibrillators (AVID) investigators: A comparison of antiarrhythmic drug therapy with implantable defibrillators in patients resuscitated from near-fatal ventricular arrhythmias. N Engl J Med. 1997;337:1576-1584.
  15. Moss AJ, Hall WJ, Cannom DS, et al, for the Multicenter Automatic Defibrillator Implantation Trial Investigators. Improved survival with an implanted defibrillator in patients with coronary disease at high risk for ventricular arrhythmia. N Engl J Med. 1996;335:1933-1940.
  16. Buxton AE, Kerry LL, Fisher JD et al, for the Multicenter Unsustained Tachycardia Trial Investigators. A randomized study of the prevention of sudden death in patients with coronary artery disease. N Engl J Med. 1999;341:1882-1890.
  17. Moss AJ, Zareba W, Hall WJ, et al, for the Multicenter Automatic Defibrillator Implantation Trial II Investigators. Prophylactic implantation of a defibrillator in patients with myocardial infarction and reduced ejection fraction. N Engl J Med. 2002;346:877-883.

  1. Kadish A, Dyer A, Daubert JP, et al, for the Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation (DEFINITE) Investigators. Prophylactic defibrillator implantation in patients with nonischemic dilated cardiomyopathy. N Engl J Med. 2004;350:2151-2158.
  2. Stiles, Steve. “SCD-HeFT: ICD Cuts All-cause Mortality by 23% in NYHA Class 2-3 Heart Failure.” 8 Mar. 2004. Web. 11 Dec. 2012.
  3. Pfeffer MA, Braunwald E. Ventricular remodeling after myocardial infarction: experimental observations and clinical implications. Circulation. 1990;81:1161-1172.
  4. St John SM, Lee D, Rouleau JL, et al. Left ventricular remodeling and ventricular arrhythmias after myocardial infarction. Circulation. 2003;107:2577-2582.
  5. Teerlink JR, Jalaluddin M, Anderson S, et al. Ambulatory ventricular arrhythmias in patients with heart failure do not specifically predict an increased risk of sudden death. Circulation. 2000;101:40-46.
  6. Moulton K, Medcalf T, Lazzara R. Premature ventricular complex morphology: a marker for left ventricular structure and function. Circulation. 1990;81:1245-1251.
  7. Vijgen J, Hill P, Lee A, et al. Tachycardia-induced cardiomyopathy secondary to right ventricular outflow tract ventricular tachycardia: improvement of left ventricular systolic function after radiofrequency catheter ablation of the arrhythmia. J Cardiovasc Electrophysiol. 1997;8:445-450.
  8. Chugh SS, Shen WK, Luria DM, Smith HC. First evidence of premature ventricular complex-induced cardiomyopathy: a potentially reversible cause of heart failure. J Cardiovasc Electrophysiol. 2000;11:328-329.
  9. Sekiguchi Y, Kazutaka A, Yasuteru Y, et al. Chronic hemodynamic effects after radiofrequency catheter ablation of frequent monomorphic ventricular premature beats. J Cardiovasc Electrophysiol. 2005;16:1057-1063.
  10. Yarlagadda RK, Iwai S, Stein KM, et al. Reversal of cardiomyopathy in patients with repetitive monomorphic ventricular ectopy originating from the right ventricular outflow tract. Circulation. 2005;112:1092-1097.
  11. Takemoto M, Yoshimura H, Ohba Y, et al. 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.
  12. European Heart Rhythm Association, Heart Rhythm Society, Zipes DP, et al. ACC/AHA/ESC 2006 guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: a report of the American College of Cardiology/American Heart Association Task Force and the European Society of Cardiology Committee for Practice Guidelines (Writing Committee to Develop Guidelines for Management of Patients With Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death). J Am Coll Cardiol. 2006;48:e247-346.
  13. Bogun F, Crawford T, Reich S, et al. Radiofrequency ablation of frequent, idiopathic premature ventricular complexes: comparison with a control group without intervention. Heart Rhythm. 2007;4:863-867.
  14. Niwano S, Wakisaka Y, Niwano H, et al. 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.

  1. Baman TS, Lange DC, Ilg KJ, et al. Relationship between burden of premature ventricular complexes and left ventricular function. Heart Rhythm. 2010;7:865-869.
  2. Jia L, Yue-Chun L, Kang-Ting J, et al. Premature ventricular contractions originating from the left ventricular septum: results of radiofrequency catheter ablation in twenty patients. BMC Cardiovasc Disord. 2011;11:27.
  3. Olgun H, Yokokawa M, Baman T, et al. The role of interpolation in PVC-induced cardiomyopathy. Heart Rhythm. 2011;8:1046-1049.
  4. Del Carpio NF, Syed FF, Noheria A, et al. 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.
  5. Yokokawa M, Kim HM, Good E, et al. Impact of QRS duration of frequent premature ventricular complexes on the development of cardiomyopathy. Heart Rhythm. 2012;9:1460-1464.
  6. Ban JE, Park HC, Park JS, et al. Electrocardiographic and electrophysiologic characteristics of premature ventricular complexes associated with left ventricular dysfunction in patients without structural heart disease. Europace. 2012 Nov 29 (Epub ahead of print)
  7. Stec S, Sikorska A, Zaborska A, et al. Benign symptomatic ventricular complexes: short- and long-term efficacy of antiarrhythmic drugs and radiofrequency ablation. Kardiol Pol. 2012;70:351-358.
  8. Yokokawa M, Good E, Crawford T, et al. Recovery from left ventricular dysfunction after ablation of frequent premature ventricular complexes. Heart Rhythm. 2012 Oct 23. (Epub ahead of print).
  9. Delgado V, Ypenburg C, van Bommel R, et al. 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.
  10. Langeland S, D’hooge J, Wouters PF, et al. Experimental validation of a new ultrasound method for the simultaneous assessment of radial and longitudinal myocardial deformation independent of insonation angle. Circulation. 2005;112:2157-2162. 
  11. Amundsen BH, Helle-Valle T, Edvardsen T, et al. Noninvasive myocardial strain measurement by speckle tracking echocardiography: validation against sonomicrometry and tagged magnetic resonance imaging. J Am Coll Cardiol. 2006;47:789-793.
  12. Wijnmaalen AP, Delgado V, Schalij MJ, et al. 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.
  13. Yao J, Xu J, Yong Y, et al. Evaluation of global and regional left ventricular systolic function in patients with frequent isolated premature ventricular complexes from the right ventricular outflow tract. Chin Med J. 2012;125:214-220.
  14. Bhushan M, Asirvatham SJ. The conundrum of ventricular arrhythmia and cardiomyopathy: which abnormality came first. Curr Heart Fail Rep. 2009;6:7-13.