Beat-to-beat T-wave amplitude variability in the risk stratification of right ventricular outflow tract-premature ventricular complex patients
Beat-to-beat T-wave amplitude variability in the risk stratification of right ventricular outflow tract-premature ventricular complex patients
Tomohide Ichikawa 2
Yoshihiro Sobue 2
Atsunobu Kasai 1
Ken Kiyono 0
Junichiro Hayano 3
Mayumi Yamamoto 2
Kentarou Okuda 2
Eiichi Watanabe 2
Yukio Ozaki 2
0 Division of Bioengineering, Graduate School of Engineering Science, Osaka University , Toyonaka , Japan
1 Division of Cardiology, Ise Red Cross Hospital , Ise , Japan
2 Department of Cardiology, Fujita Health University School of Medicine , 1-98 Dengakugakubo, Kutsukake-cho, Toyoake, Aichi 470-1192 , Japan
3 Department of Medical Education, Nagoya City University Graduate School of Medical Sciences , Nagoya , Japan
Aims Premature ventricular complexes (PVCs) originating from the right ventricular outflow tract (RVOT) may occasionally trigger monomorphic ventricular tachycardia (MVT), polymorphic ventricular tachycardia (PVT), or ventricular fibrillation (VF). We examined whether an analysis of the ventricular repolarization instability could differentiate PVT/VF triggered by RVOT-PVCs from benign RVOT-PVCs or MVT. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Methods We evaluated the ventricular repolarization instability as assessed by the beat-to-beat T-wave amplitude variability (TAV) using Holter recordings in patients with RVOT-PVCs but with no structural heart disease. We determined the prematurity index, defined as the ratio of the coupling interval of the first ventricular tachycardia (VT) beat or isolated PVC to the preceding R - R interval just before the VT or isolated PVC in the Holter recordings. The study patients were classified into RVOT-PVCs/MVT (n ¼ 33) and PVT/VF (n ¼ 10). . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Results The two groups did not differ with respect to the age, sex, and left ventricular ejection fraction. There was no significant difference in the prematurity index between the two groups (RVOT-PVCs/MVT 0.66 + 0.16 vs. PVT/VF 0.61 + 0.13, P ¼ 0.60). The patients with PVT/VF had a significantly larger maximum TAV than those with RVOT-PVCs/MVT (31 + 13 vs. 68 + 40 mV, P , 0.001). Patients with a higher than median value of the TAV (33 mV) were at increased risk of PVT/VF vs. those with a lower than median value, after adjusting for the age and sex [9.25 (95% confidence interval: 1.27 - 19.2); P ¼ 0.03]. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . Conclusions The TAV analysis is a useful measure to identify the subset of usually benign RVOT-PVC/MVT patients prone to PVT/VF. - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -
Premature ventricular complexes (PVCs) originating from the right
ventricular outflow tract (RVOT) are one of the more common ventricular
arrhythmias.1 Right ventricular outflow tract-premature ventricular
complexes are frequently observed in patients who have no structural
heart disease and are considered benign even when they develop into
monomorphic ventricular tachycardia (MVT).2 Nevertheless, one
occasionally comes across lethal polymorphic ventricular tachycardia (PVT)
or ventricular fibrillation (VF) triggered by RVOT-PVCs.3 – 7
The mechanism of RVOT-ventricular tachycardia (VT) is typically
triggered activity caused by a calcium overload via a cyclic adenosine
monophosphate mediated process.8 Therefore, various investigators
have focused on the role that short RVOT-PVC coupling intervals
might play in triggering PVT/VF; however, the triggering coupling
interval values reported vary widely.3 – 6 Recently, Igarashi et al.7
reported that the prematurity index or QT index4 could differentiate
PVT/VF triggered by RVOT-PVCs from MVT.
The pathophysiology of ventricular tachyarrhythmias is believed to
require both a triggering event, and underlying temporal and spatial
† Premature ventricular complexes (PVCs) originating from the
right ventricular outflow tract (RVOT) are one of the most
common arrhythmias and are generally considered benign.
Nevertheless, a subset develops into lethal polymorphic
ventricular tachycardia (PVT) or ventricular fibrillation (VF).
† Up to now, coupling interval of the triggering PVC,
prematurity index, and QT index was useful markers to identify the
subset of patients with RVOT-PVCs prone to PVT/VF.
† We found that for the first time an increased beat-to-beat
T-wave amplitude variability in the Holter electrocardiogram
might identify the subset of patients with RVOT-PVCs prone
dispersion of the repolarization. The T-wave alternans (TWA)
phenomenon, beat-to-beat alteration in the morphology, and amplitude
of the T-wave have long been recognized and linked to
arrhythmogenesis.9,10Among the non-invasive risk stratifiers, the
frequencydomain technique for the assessment of TWA is an established
measure for the prediction of VT/VF in diverse heart diseases.10
Recently, Couderc et al.11 developed a novel approach to determine
the beat-to-beat T-wave amplitude variability (TAV) obtained from
the Holter electrocardiogram (ECG). They demonstrated that an
increased TAV was associated with an increased risk for VT assessed
by the frequency of implantable cardioverter-defibrillator (ICD)
anti-tachycardic therapies in post-infarction patients with severe
left ventricular dysfunction. Subsequent studies have shown that
an increased TAV is also observed in patients with various heart
diseases.12,13 The aim of this study was to test the hypothesis that
the TAV is a useful parameter for the identification of the subset of
patients with RVOT-PVCs prone to PVT/VF and differentiate them
from the benign RVOT-PVC and MVT patients.
We prospectively enrolled 43 consecutive RVOT-PVC patients
without any structural heart disease who underwent 24 h Holter
ECG recordings from May 2008 to December 2013. We classified
the patients into two groups: RVOT-PVC/MVT and PVT/VF. We
first screened the RVOT-PVC patients who had PVCs appearing in
all 12 ECG leads simultaneously to determine the origin based on
the algorithm shown in the previous report.14 We excluded the
patients with structural heart disease on the basis of the medical
history, physical examination, laboratory data, echocardiography,
and coronary angiography. Arrhythmogenic right ventricular
cardiomyopathy was excluded in the PVT/VF patients according to the task
force criteria.15 Brugada syndrome was excluded by the absence of a
Brugada-pattern ECG after flecainide provocation and the absence of
a family history of sudden death at a young age in the all PVT/VF
patients. We also excluded patients with long-QT syndrome and
J wave syndrome. We excluded patients with atrial fibrillation
because the utility of the TAV analysis was untested in such patients.
The study protocol was approved by the Institutional Review Board
and all patients gave their written informed consent.
A single electrocardiographic technician blinded to any of the clinical
information of the patients analysed the ECG measurements. We
determined the following ECG parameters from both the 12-lead
ECG at rest and Holter recording during isolated PVCs or episodes
of VT: (i) the sinus cycle length just before isolated PVCs or VT;
(ii) coupling interval, defined as the R – R interval between isolated
PVCs or PVCs initiating VT and the preceding sinus complex; (iii)
prematurity index,4 defined as the ratio of the coupling interval to the
preceding sinus R – R interval [i.e. value of (ii)/value of (i)]; and
(iv) the QT index,4 defined as the ratio of the coupling interval to
the QT interval of the preceding sinus complex. We examined
the polarity of the PVC in lead I and defined it as positive if there
was a positive deflection exceeding the negative component by an
amplitude of .0.1 mV.16 Ventricular tachycardia was considered
present when at least three consecutive PVCs occurred at a rate of
.120 beats/min. Polymorphic ventricular tachycardia was defined
as VT with more than five consecutive beats with different QRS
morphologies.5 Ventricular fibrillation required a disorganized
ventricular rhythm with no discrete QRS complexes. The PVT/VF
episodes were obtained from Holter recordings or automated
external defibrillators during cardiopulmonary resuscitation, and
monitor ECGs recorded on the wards.
Holter electrocardiogram recordings and
analysis of the T-wave amplitude variability
Digital 24 h Holter ECG recordings (SpiderView, Ela Medical, Sorin
Group, Le Plessis Robinson, France) were sampled at 1 kHz with a
resolution of 2.5 mV. The electrodes (Blue Sensor, Ambu, Ballerup,
Denmark) were placed in an orthogonal X, Y, and Z lead
configuration. The Holter data were manually edited to eliminate any
ectopic beats and signal noise and then analysed for the conventional
heart rate variability parameters, dynamic heart rate variability
indices including the deceleration capacity,17 non-Gaussian index,18
heart rate turbulence,19 and signal-averaged ECG.20 The detailed
method for measuring the TAV has been reported elsewhere.11,12
SyneTVar 3.10b software (Ela Medical, Sorin Group) was used
for the analysis of the TAV based on the vector magnitude of
VM ¼ pX2 + Y2 + Z2, where VM was used as the primary lead for
the analysis. The software automatically selects a cluster of 60
QRS-T consecutive complexes for the analysis (Figure 1). The clusters
were excluded from analysis in case of (i) the presence of atrial and
ventricular ectopy, (ii) high R – R interval variability defined as the
presence of R – R intervals .20 or ,20% from the mean, and (iii) a
noise level exceeding 10 mV. The variance of the TAV (in mV),
defined as the average of the squared deviations from the mean,
was assessed on each of eight consecutive 50 ms T-wave segments
(TAV 1 – TAV 8) following the QRS offset (defined as the QRS
onset +120 ms) for a given cluster. The mean TAV was defined as
the average TAV from T-wave segments 1 – 8, and the max TAV as
the maximum TAV from T-wave segments 1 – 8. Finally, each
patient had a mean TAV that was the mean value of the TAV from
all clusters of the recording and had a max TAV that was defined as
Figure 1 T-wave amplitude variability. A set of 60 continuous
sinus beats is identified and aligned based on beginning of the
QRS and the T wave is windowed using a 50 ms duration interval.
Upper panels: the oblique view of 60 consecutive T waves. Lower
panels: transverse views of the 60 consecutive T waves. The
control subject exhibited a small variation in the T-wave amplitude
(10 mV in this case), but the ventricular fibrillation patient had a
large variation in the T-wave amplitude (81 mV in this case).
the maximum TAV value of all the clusters. Uninterpretable clusters
were carefully deleted by visual inspection. To assess the
reproducibility of the TAV analysis, all 43 recordings were interpreted at an
interval of 1 month, resulting in a correlation coefficient of 0.95.
Holter ECGs were recorded before the administration of any
Electrophysiologic evaluation and
radiofrequency catheter ablation
An electrophysiologic evaluation and radiofrequency catheter
ablation (RFCA) targeting the triggering PVC was attempted before the
administration of amiodarone or after withdrawal of other
antiarrhythmic drugs for more than five times the half-life. The surface
ECGs and bipolar endocardial electrograms were continuously
monitored and stored on a computer-based digital amplifier/recorder
system (LabsystemTM Pro, Bard Electrophysiology, Lowell, MA,
USA). Intracardiac electrograms were filtered from 30 to 500 Hz.
The CartoTM system (Biosense-Webster, Diamond Bar, CA, USA)
or EnSiteTM ArrayTM mapping system (St. Jude Medical, St. Paul,
MN, USA) was used for the 3D electroanatomical mapping. Steerable
quadripolar electrode catheters were introduced into the His bundle
region and RV apex, and a decapolar catheter (5 mm electrode
spacing, St. Jude Medical) was positioned within the coronary sinus
via the right femoral vein. A 7-Fr quadripolar electrode catheter
with a 4 mm distal electrode and a deflectable tip (SafireTM BLUTM
or TherapyTM Cool FlexTM, St. Jude Medical) was used for mapping
and ablation. Programmed stimulation was performed with up to
three extrastimuli from the RV apex and RVOT, and isoproterenol
was used in an effort to induce VT. The site of the PVC origin
was defined as the site where the earliest ventricular
activation was recorded and/or a perfect pace map was obtained, and
radiofrequency energy was delivered at that site. The radiofrequency
energy was a maximum power of 30 W, maximum temperature of
408C, and duration of up to 60 s for each delivery. Successful
RFCA was defined as the absence of any spontaneous or induced
clinical VT/PVCs, both in the absence and presence of isoproterenol, at
the end of the procedure.
Differences between the two groups were evaluated using a
Student’s t-test for continuous variables and the x 2 test for categorical
data. A multiple regression analysis was used to test the relationship
between the heart rate variability index, heart rate turbulence, and
TAV. A multivariate logistic analysis adjusted by the age and sex
was performed to test the predictive value of the TAV for PVT/VF.
Data are presented as the mean + SD. A P-value of , 0.05 was
considered as statistically significant. The statistical analyses were
performed using JMP10.0.2 software.
The baseline characteristics classified according to the type of
arrhythmia are summarized in Table 1. No significant differences
were found in regard to the age, sex, comorbidities, and left
ventricular ejection fraction between the RVOT-PVC/MVT patients and PVT/
VF patients. No patients had a family history of sudden death. We
found no significant difference in the prevalence of a positive QRS
in lead I between the two groups. There were no significant
differences in the coupling interval, prematurity index, and QT index
in the 12-lead ECG between the two groups. Also, there were no
significant differences in the QRS duration, R wave duration index, and
R/S wave amplitude index, and the QRS morphology of the PVCs met
the RVOT origin criteria. The clinical profiles of the 10 PVT/VF
patients are presented in Table 2. Two patients with PVT/VF also
had episodes of MVT with a cycle length of ≤300 ms (Patients #4
and #6, Table 2), and they were analysed as PVT/VF patients.
A representative case of PVT/VF recorded on the Holter ECG is
shown in Figure 2.
Holter electrocardiogram parameters
Table 3 summarizes the Holter ECG data. The heart rate variability
index and heart rate turbulence were determined in all patients.
The TAV results were interpretable in 43 of 52 patients (83%),
whose atrial (n ¼ 1) or ventricular (n ¼ 4) premature complexes,
or paroxysmal atrial fibrillation (n ¼ 4) precluded the TAV
measurement. We analysed 1696 + 95 clusters in the study patients. There
were no significant differences in the heart rate, conventional heart
rate variability parameters, dynamic heart rate variability indices
including the deceleration capacity, non-Gaussian index, heart rate
turbulence, or signal-averaged ECG. A multiple regression analysis
revealed that there were no significant associations between the
heart rate variability index, heart rate turbulence, and TAV (see
Supplementary material online, Table S1). The PVT/VF patients tended to
have fewer PVCs (P ¼ 0.07) and a relatively higher number of PVC
morphologies (P ¼ 0.07) compared with the RVOT-PVC/MVT
patients. The coupling interval in the PVT/VF patients was shorter
Data represent the means + SD or frequency.
RVOT, right ventricular outflow tract; PVC, premature ventricular complex; MVT, monomorphic ventricular tachycardia; PVT, polymorphic ventricular tachycardia; VF, ventricular
fibrillation; LVEF, left ventricular ejection fraction; RFCA, radiofrequency catheter ablation; ICD, implantable cardioverter-defibrillator; QTc, rate-corrected QT interval by Bazett’s
than that in the RVOT-PVC/MVT patients (P ¼ 0.03). There were no
significant differences in the prematurity index and QT index
between the two groups. The PVT/VF patients exhibited a
significantly higher value of the max TAV than patients with RVOT-PVC/MVT
(P , 0.001). The distribution of the max TAV across the
repolarization intervals is presented in a Supplementary material online, file.
The max TAV was frequently recorded at the peak of the T-wave.
When patients were dichotomized by a median value of the TAV of
33 mV, patients with a higher than median value were at increased
risk of PVT/VF vs. those with a lower than median value after
adjusting for the age and sex [9.25 (95% confidence interval: 1.27 – 19.2);
P ¼ 0.03]. Thus, the sensitivity and specificity for predicting PVT/VF
were 90.0 and 60.6%, respectively. The coupling interval was not
predictive of PVT/VF [4.76 (95% confidence interval: 0.83 – 39.1);
P ¼ 0.08].
Treatment and follow-up
Radiofrequency catheter ablation targeting the triggering PVCs was
performed (Table 1). Ventricular fibrillation was induced in one
patient with PVT/VF (Patient #8, Table 2) with three extrastimuli
from the RV apex in the absence of isoproterenol, and an
isoproterenol infusion alone induced MVT in one MVT patient. There
was no significant difference in the location of the origin of the
triggering PVC between the two groups. Endocardial mapping presented no
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local abnormal ECGs including fragmentation or delayed potentials.
After the RFCA for the initial targeted PVC, a PVC with a different
QRS morphology appeared in one patient in the PVT/VF group
(Patient #4, Table 2). A further energy delivery 1 cm above this
site abolished another form of PVCs. Partial success was achieved
in Patient #5 since the triggering PVC occurred very infrequently,
and the induction of the PVC or PVT/VF was difficult. We also
confirmed that no perfect pace maps were obtained in the left ventricular
outflow tract, pulmonary artery, or aortic cusps. The mean bipolar
local activation time at the successful RFCA site was 35 + 12 ms
before the surface QRS onset. No significant difference was observed
in the RFCA success rate between the two groups. Implantable
cardioverter-defibrillators were implanted in five patients with
PVT/VF, but the remaining five patients refused to undergo an ICD
implantation. An appropriate shock for VF was delivered in Patient
#2, in whom RFCA was refused. No patients died during a mean
follow-up of 28 + 10 months.
The electrophysiological mechanisms responsible for enhanced
susceptibility to life-threatening arrhythmias in RVOT-PVC patients
without structural heart disease are not well understood. We
observed that the prematurity index and QT index failed to
differentiate the subset of patients with RVOT-PVCs prone to PVT/VF from
the RVOT-PVC/MVT patients. We found that for the first time that
the increased repolarization lability as assessed by the TAV was
predictive of PVT/VF.
Previous studies have suggested that short coupling intervals of
triggering PVCs are responsible for the development of PVT/VF,
regardless of the location of the focus.2 Leenhardt et al.3 showed
that short-coupled PVCs (a coupling interval of 245 + 28 ms)
might be related to PVT/VF, which was referred to as a ‘variant of
torsade de pointes.’ Subsequent authors have reported that PVT/
VF can be triggered by intermediately coupled RVOT-PVCs,4,6 or
even longer RVOT-PVC coupling intervals5,7 trigger the
development of PVT/VF. Therefore, a ‘short’ coupling interval alone may
be a poor predictor of whether an RVOT-PVC is benign or possibly
lethal. In this study, the coupling interval in the PVT/VF patients
was shorter than that in the RVOT-PVC/MVT patients, but the
predictive accuracy of the coupling interval was low compared with the
The smaller prematurity index and the QT index have been shown
to be associated with the initiation of PVT or VF.4 Igarashi et al.,7 who
examined the prematurity index between patients with MVT and
PVT arising from RVOT-PVCs, found that a smaller prematurity
index was able to differentiate between MVT and PVT. In this
study, however, we found that there were no significant differences
in the prematurity index and the QT index between the two groups.
The PVT/VF patients tended to have a greater number of PVC
morphologies than the RVOT-PVC/MVT patients. In addition, two
patients with PVT/VF had both episodes of PVT/VF and MVT,
suggesting we may not have been able to exclude an undiagnosed
cardiomyopathic process contributing to the arrhythmias in the PVT/VF
In this study, the average number of PVCs during the Holter
recordings was relatively smaller in the RVOT-PVC/MVT patients
than those with PVT/VF. We have no clear explanation for our
observation, but the study by Viskin et al.6 showed that the total
number of PVCs was relatively greater in those with benign
RVOT-VT than those with short-coupled RVOT-VT or idiopathic
VF. Moreover, Leenhardt et al.3 reported that the total number of
PVCs in the eight patients with a short-coupled variant of torsades
de pointes was 846 + 1473 per day, which was less than our
We found that an increased TAV was associated with the PVT/VF
patients, suggesting that an arrhythmogenic substrate exists in the
ventricles, but we could not diagnose whether there was a
repolarization abnormality localized to the RVOT area or not. It may be
helpful if we could assess the repolarization process in the RVOT
The TAV, in addition to TWA9 and the QT interval variability,21 has
been described as a promising new technique for the quantification of
ventricular repolarization instability and the stratification of the
arrhythmic risk in various heart diseases.11 –13 We previously examined the TAV
in the survivors of VT/VF without evidence of structural heart disease.22
The cut-off value for the max TAV in that study was 38 mV,22 which was
similar to this study (median 33 mV). Extramiana et al.12 reported that
the max TAV in long-QT patients was 46 mV, lower than the 58 mV
cut-off value determined by Couderc et al.11 for the MADIT II study
population with an ICD therapy endpoint. These observations suggest
that the optimal cut-off value for the TAV for the risk stratification
should be determined by the underlying heart disease.
Recently, newly developed time-domain techniques such as the
modified moving average TWA,23 in addition to conventional spectral
methods,9 have been proven to be useful measures to stratify high-risk
patients among the diverse underlying heart diseases. The strength
of the TWA is that it has experimental background and extensive
clinical evidence. The TAV, a conceptually similar measure, has been
developed as a quantitative approach that assesses subtle ventricular
repolarization abnormalities. Although much clinical evidence has
been provided,11– 13,22 no experimental study has clarified the
electrophysiologic mechanism of the TAV. In addition, some technical
difficulties are associated with the TAV measurements. The TAV
should be measured by the orthogonal X, Y, Z leads, and interpretable
when patients have a lower noise level, stable R – R interval, and
no premature complexes in the 60-beat clusters. Future study is
required to test whether the TAV and TWA are independent or
complementary markers for risk stratification.
Endocardial repolarization alternans was shown to have good
concordance with the TWA measured on the surface ECG.24 Recently,
Heart rate turbulence
Positive, n (%)
Max TAV (mV)
Mean TAV (mV)
21.6 + 2.0
6.3 + 4.6
Maury et al.25 examined the beat-to-beat variations in the T-wave
morphology before the spontaneous VT/VF onset in ICD-stored
intracardiac electrograms. They found that several parameters
characterizing the T-wave (amplitude, shape, or duration) varied greater
immediately before VT/VF than during the reference. In addition to
estimate the ventricular repolarization instability of the baseline
using TAV, short-term prediction of VT/VF onset is an important
area for the development of future preventive therapeutic options
in this setting.
A previous report by Leenhardt et al.3 suggests that patients with
short-coupled PVCs have a depressed heart rate variability; however,
very limited data are available on the autonomic modulation in
RVOT-PVC patients. In this study, we showed that there were no
significant differences in the heart rate variability, and heart rate
turbulence parameters among the patient groups, suggesting that
autonomic modulation may have a lesser influence on the occurrence of
PVT/VF in RVOT-PVC patients.
In this study, RFCA was performed in 8 of 10 patients with PVT/VF
to eliminate the triggering PVC. We observed that RFCA of one focus
was followed by the onset of a new PVC morphology in Patient #4
(Table 2). This finding was consistent with the previous report.5
Indeed, Noda et al.5 have shown that rapid pacing from the
responsible RVOT area gives rise to a polymorphic morphological change
in the QRS configuration. Therefore, they proposed that functional
block and/or delayed conduction by rapid firing arising from a local
focus at the RVOT lead to fibrillatory conduction, causing PVT or
VF without an organic delayed conduction zone. If PVT/VF is
caused by a trigger acting on a substrate with dispersion of the
repolarization, RFCA alone which removes the trigger but not the
substrate, may not guarantee the long-term prevention of PVT/VF. We
also believe that in the future, those RVOT-PVCs in patients who
exhibit a greater TAV may guide the ICD implantation.
Our analysis was based on observations from a small sample size at
only two institutions. A larger study designed to evaluate the TAV
cut-off values for discriminating between benign and possibly lethal
RVOT-PVCs would be required. The RVOT-PVCs/MVT may also
be observed in the patients with arrhythmogenic right ventricular
cardiomyopathy or Brugada syndrome, but we did not rule out
these possibilities. The RVOT-PVCs are generally considered as a
benign type of arrhythmia and more prevalent. In this study,
however, the prevalence of RVOT-PVCs was relatively lower than
PVT/VF. This probably represents a referral bias, because patients
with PVT/VF are more likely to be hospitalized or referred for
aggressive treatments such as RFCA or ICD implantations, whereas
RVOT-PVC patients are more likely to be treated conservatively
as outpatients and have a lesser chance of undergoing Holter
The TAV, an analysis of ventricular repolarization instability, may be a
useful measure for differentiating patients prone to PVT/VF triggered
by RVOT-PVCs from benign RVOT-PVCs or MVT.
Supplementary material is available at Europace online.
The authors thank Ms Akemi Yamauchi for analysing the ECG data
and Dr Mari Alford Watanabe and Mr John Martin for preparing
Conflict of interest: none declared.
This study was supported by the Suzuken Memorial Foundation and
JSPS KAKENHI grant numbers 23700544 and 26461094.
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