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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).
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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
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February 2012
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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.
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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
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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.
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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.
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Circ Arrhythm Electrophysiol
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Table.
Effects of Catheter Ablation of PVCs on Cardiac Function
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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.
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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
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Circ Arrhythm Electrophysiol. 2012;5:229-236
doi: 10.1161/CIRCEP.111.963348
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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