Predictors of adverse outcome in patients with
frequent premature ventricular complexes: The ABC-VT
risk score
Aleksandr Voskoboinik, MBBS, PhD,*1 Alexios Hadjis, MD, FHRS,*1
Christina Alhede, MD,* Sung Il Im, MD, PhD,*† Hansu Park, MD,†
Joshua Moss, MD, FHRS,* Gregory M. Marcus, MD, FHRS,* Henry Hsia, MD, FHRS,*
Byron Lee, MD,* Zian Tseng, MD,* Randall Lee, MD, PhD,* Melvin Scheinman, MD,*
Vasanth Vedantham, MD,* Eric Vittinghoff, PhD,* Kyoung-Min Park, MD, PhD,‡
Edward P. Gerstenfeld, MD, FHRS*
From the *Division of Cardiology, University of California San Francisco, San Francisco, California,
†
Division of Cardiology, Kosin University Gospel Hospital, Busan, Republic of Korea, and ‡Division of
Cardiology, Samsung Medical Center, Seoul, Republic of Korea.
BACKGROUND No independently validated score currently exists
for risk stratification of patients with frequent premature ventricu-
lar complexes (PVCs).
OBJECTIVES The purpose of this study was to develop a risk score
to predict adverse events in patients with frequent PVCs.
METHODS We analyzed consecutive patients between 2012 and
2017 undergoing 14-day continuous monitoring with frequent
PVCs (.5%) and concurrent echocardiography. We performed bi-
nary logistic regression to determine multivariate predictors of
adverse left ventricular remodeling (left ventricular ejection frac-
tion [LVEF] ,45% or left ventricular end-diastolic volume index
.75 mL/m2). A risk score was created using the log(odds ratio
(OR)) of these predictors and validated prospectively to determine
the risk of future adverse events in those with baseline LVEF .45%.
An adverse event was defined as LVEF decline by 10%, heart failure
hospitalization, or cardiovascular mortality. Two validation cohorts
were used: follow-up from the original derivation cohort (cohort 1)
and an independent Korean PVC registry (cohort 2).
Introduction
Patients with frequent premature ventricular complexes
(PVCs) may present a diagnostic and management challenge
for clinicians. In some patients, PVCs may be the first mani-
festation of undiagnosed structural heart disease, while in
others they may cause or worsen cardiomyopathy if ectopic
Dr Voskoboinik was partially funded by a fellowship grant from the
Heart Rhythm Society. Dr Alhede was funded by a Fulbright scholarship.
1
Joint first authors. Address reprint requests and correspondence:
Dr Edward P. Gerstenfeld, Department of Cardiac Electrophysiology, Uni-
versity of California San Francisco, 500 Parnassus Avenue, San Francisco,
CA 94143. E-mail address: Edward.Gerstenfeld@ucsf.edu.
1547-5271/$-see front matter © 2020 Heart Rhythm Society. All rights reserved.
RESULTS The derivation cohort comprised 206 patients with a
mean PVC burden of 11.6% 6 6.2% and considerable daily fluctua-
tion (minimum burden 7.3% 6 6.2% vs maximum 17.9% 6 8.0%).
Independent predictors of adverse remodeling were as follows: su-
periorly directed PVC axis (OR 2.7; 1 point), PVC burden 10%–20%
(OR 3.5; 2 points) and .20% (OR 4.4; 3 points), PVC coupling inter-
val .500 ms (OR 4.7; 4 points), nonsustained ventricular tachy-
cardia (OR 5.3; 4 points), which form the ABC-VT risk score. This
score predicted future adverse events in both validation cohorts:
cohort 1, hazard ratio 1.43; 95% confidence interval 1.19–1.73;
P , .001 and cohort 2, hazard ratio 1.22; 95% confidence interval
1.05–1.42; P 5 .01.
CONCLUSION The ABC-VT score is a simple tool that predicts
adverse left ventricular remodeling and future clinical deterioration
in patients with frequent PVCs.
KEYWORDS Cardiomyopathy; Left ventricular remodeling; Prema-
ture ventricular complexes; Risk score; Ventricular tachycardia
(Heart Rhythm 2020;17:1066–1074) © 2020 Heart Rhythm Society.
All rights reserved.
burden is sufficiently high.1,2 While antiarrhythmic medica-
tions3 and catheter ablation4,5 have been shown to improve
systolic function and exercise capacity6 in those with
PVC-induced cardiomyopathy, the treatment of patients
with frequent PVCs and preserved left ventricular (LV) func-
tion is controversial. Spontaneous reduction over time has
been reported in some of these patients,7 potentially obvi-
ating the need for antiarrhythmic medications and/or invasive
ablation.
While PVC burden remains the most widely accepted pre-
dictor of the development of PVC-mediated cardiomyopathy
and clinical deterioration,2,8 other risk factors are less well
defined. We sought to determine clinical and
https://doi.org/10.1016/j.hrthm.2020.02.020
Voskoboinik et al ABC-VT Risk Score for Frequent PVCs 1067

electrocardiographic (ECG) variables associated with Table 1 Baseline characteristics of the derivation cohort
adverse LV remodeling with the aim of devising a risk score (N 5 206)
to assist clinicians with decision making, particularly in those Parameter Value
with relatively preserved LV function.
Clinical
Male sex 127 (62)
Age (y) 65 6 16
Methods Body mass index (kg/m2) 27 6 6
Risk score derivation Hypertension 107 (52)
We retrospectively analyzed 206 consecutive patients Coronary artery disease 56 (27)
between 2012 and 2017 undergoing continuous 14-day Valvular heart disease 38 (18)
Atrial fibrillation 36 (17)
ECG patch monitoring (Zio patch, iRhythm, San Francisco, NYHA class 1.36 6 0.63
CA) who had an elevated burden of PVCs (average daily Medications
burden .5%). All patients also underwent transthoracic b-Blockers 90 (44)
echocardiography within 3 months of the patch monitoring Calcium channel blockers 28 (14)
period. Echocardiograms were performed using commer- Class I or III antiarrhythmic agents 7 (3)
Echocardiographic
cially available equipment and standard techniques. Left ven- LVEF (%) 57 6 12
tricular ejection fraction (LVEF) was assessed using the LVEDVI (mL/m2) 63 6 23
Simpson’s disc method in the apical 4-chamber view and LVESVI (mL/m2) 29 6 19
interpreted by experienced echocardiographers. LV volumes LAVI (mL/m2) 36 6 16
were measured according to the American Society of Echo- Electrocardiographic
PVC QRS duration (ms) 151 6 19
cardiography guidelines and indexed for body surface area. PVC coupling interval (ms) 547 6 85
For each patient, we collected demographic and clinical Post-PVC coupling interval (ms) 1051 6 198
data from the electronic medical record, reviewed 12-lead Ventricular tachycardia 122 (59)
ECGs to assess PVC morphology and PVC QRS duration, Ventricular bigeminy 83 (40)
and performed digital signal processing of raw 14-day single Minimum 24-h PVC burden (%) 7.3 6 6.2
Mean 24-h PVC burden (%) 11.6 6 6.2
lead patch electrogram data (sampled at 240 Hz) using Maximum 24-h PVC burden (%) 17.9 6 8.0
custom-designed software (MATLAB, MathWorks, Natick, Maximum – minimum daily PVC 10.6 6 5.6
MA). The custom-designed software analyzed the raw burden (%)
ECG data in several steps: (1) QRS detection, (2) differenti- Number of PVC morphologies 1.9 6 1.0
ation of PVCs from normally conducted beats, (3) calculation Multiple PVC morphologies (%) 55
LBBB morphology (%) 60
of each pre-PVC coupling interval to the prior sinus beat, (4) Inferiorly directed axis (%) 65
calculation of each post-PVC coupling interval to the next si- Left ventricular location 62
nus beat, (5) calculation of the number of different PVC mor- Apical location (%) 13
phologies (based on PVC correlation coefficient ,0.9), and Values are presented as mean 6 standard deviation or as n (%).
(6) calculation of any runs of nonsustained ventricular tachy- LAVI 5 left atrial volume index; LBBB 5 left bundle branch block; LVEDVI
cardia (NSVT) and duration. Summary data were then calcu- 5 left ventricular end-diastolic volume index; LVEF 5 left ventricular ejec-
lated for each patient, including the mean PVC coupling tion fraction; LVESVI 5 left ventricular end-systolic volume index; NYHA
interval and standard deviation, mean post-PVC coupling in- 5 New York Heart Association; PVC 5 premature ventricular contraction.
terval and standard deviation, daily PVC burden (including
minimum, mean, maximum, and variance), presence of
NSVT, and presence of atrial fibrillation. Dominant PVC 2 cardiologists who were blinded to clinical and echocardio-
QRS duration for each patient was measured using digital graphic data.
calipers on a standard 12-lead ECG and measured from the We then used logistic regression to estimate unadjusted
onset of the QRS complex in any lead until the latest offset associations of these candidate predictors with adverse LV
in any lead. The PVC axis was classified as “superior” or remodeling (LVEF ,45% or left ventricular end-diastolic
“inferior” on the basis of the dominant deflection in lead II volume index .75 mL/m2) in the entire cohort. Those with
being either negative (superior axis) or positive (inferior statistically significant unadjusted associations (P , .05)
axis), regardless of the ventricle of origin. If lead II was “iso- were included in the final model. One to 4 points were as-
electric,” lead III followed by aVF was used. Basal origin was signed to each variable, in proportion to its coefficient (ie,
characterized by dominant R waves in leads V4 through V6 the log(odds ratio) [OR]) in the final adjusted model, and
and apical origin by dominant S waves in leads V4 through then summed to obtain the risk score. To be compatible
V6. LV origin was suggested by either a right bundle branch with point score transformation, PVC burden was catego-
block pattern in lead V1 or left bundle branch block with fea- rized as ,10%, 10%–20%, and .20%.
tures consistent with LV outflow tract origin (prominent r/
Rwave amplitude and/or V2 transition ratio .0.6). Ventricu- Risk score validation
lar tachycardia (VT) was defined as .3 beats of ventricular To validate the risk score, we assessed its associations with
origin at .100 beats/min. ECG analyses were performed by outcomes at follow-up in both a healthy subset of the original
1068 Heart Rhythm, Vol 17, No 7, July 2020

Figure 1 Variability between the lowest 24-hour premature ventricular contraction (PVC) burden (minimum) and the highest 24-hour PVC burden (maximum)
throughout the 14-day monitoring period.

derivation cohort (cohort 1) and an independent cohort Results

(cohort 2) from a Korean PVC registry.9,10 In cohort 1, med- In total, 206 consecutive patients were included in the deriva-
ical records for the subgroup of patients with LVEF .45% at tion cohort, with baseline clinical, ECG, and echocardio-
baseline were reviewed from study entry until October 2019. graphic characteristics listed in Table 1. The majority of
Cohort 2 comprised consecutive patients attending Kosin patients were male 127 (62%) with mean age 65 6 16 years.
University Gospel Hospital (Busan, South Korea) and Sam- Hypertension was the most common medical comorbidity
sung Medical Center between 2006 and 2015 with mean 107 (52%). One hundred sixty-seven (81%) patients had pre-
PVC burden .5% on 24-hour Holter and LVEF .45%. In served LVEF (.45%) and 39 (19%) had reduced LVEF
addition to LVEF criteria, patients with structural heart dis- (,45%); the majority were not on antiarrhythmic medica-
ease (including fibrosis on cardiac magnetic resonance imag- tions. Most patients had .1 PVC morphology (55%), with
ing) were excluded from both validation cohorts. In both the dominant morphology most commonly being LV in
cohorts, an adverse event was defined as a composite of car- origin (62%) with an inferiorly directed axis (65%). The
diovascular mortality, absolute LVEF decline by 10% (with mean PVC QRS duration was 151 6 19 ms.
LVEF ,50%), or heart failure hospitalization on the basis The total patch wear time was 11.7 6 3.3 days. The mean
of including echocardiograms, inpatient admissions, and PVC burden was 11.6% 6 6.2%; however, there was
outpatient visits. A slightly lower baseline LVEF cutoff of
.45% was used to define “preserved systolic function” at
baseline, as in other studies,11,12 and a relatively large Table 2 PVC burden—univariate predictors of adverse LV
LVEF drop (10%) to meet the criteria for an adverse event remodeling (LVEF ,45% or LVEDVI .75 mL/m2)
to account for discrepancy in LVEF measurement(s) due to
Univariate analysis
ectopy. Cox proportional hazards models were used to assess
the utility of the risk score in predicting future adverse events Parameter OR 95% CI P
in both validation cohorts. Minimum PVC burden 1.07 1.02–1.12 .009
Continuous variables were summarized using mean and Mean PVC burden 1.06 1.01–1.11 .02
standard deviation (normally distributed) or median and in- Maximum PVC burden 1.05 1.01–1.08 .02
terquartile range (skewed), while categorical variables were Day 1 PVC burden 1.04 1.00–1.08 .03
PVC burden 10%–20%* 2.20 1.05–4.62 .04
summarized as count (proportion), with independent groups PVC burden .20%* 3.47 1.15–10.48 .03
compared using the c2 test. Data analysis was performed us- Maximum – minimum burden 1.0 1.0–1.0 .52
ing SPSS version 26 (IBM Corporation, Armonk, NY). Daily PVC variance 1.0 0.98–1.01 .61
P values ,0.05 were considered statistically significant. CI 5 confidence interval; LV 5 left ventricular; OR 5 odds ratio. Other
The study was approved by the local institutional review abbreviations as in Table 1.
board of participating institutions. *Using minimum 24-h burden over the 14-d monitoring period.
Voskoboinik et al ABC-VT Risk Score for Frequent PVCs 1069

Table 3 Multivariate predictors of adverse LV remodeling (LVEF ,45% or LVEDVI .75 mL/m2)
Univariate analysis Multivariate analysis
Parameter OR 95% CI P OR 95% CI P
NSVT 6.19 2.8–15.2 ,.001 5.26 2.09 – 13.23 ,.001
PVC coupling interval .500 ms 4.67 2.4–9.0 ,.001 4.73 2.19 – 10.21 ,.001
Superiorly directed PVC axis 2.27 1.4–4.8 .004 2.70 1.25 – 5.81 .01
PVC burden 10%–20%* 2.20 1.1–4.6 .04 3.50 1.39 – 8.82 .01
PVC burden .20%* 3.47 1.2–10.5 .03 4.40 1.17 – 16.49 .03
Broad PVC QRS (.160 ms) 2.03 1.0–4.4 .07 – – –
LBBB morphology PVC 0.60 0.3–1.2 .12 – – –
Right ventricular origin PVC 1.05 0.6–2.0 .88 – – –
Basal origin PVC 0.53 0.2–1.3 .17 – – –
Age 1.00 1.0–1.0 .98 – – –
Male sex 1.93 1.0–3.7 .05
Atrial fibrillation 1.93 0.9–4.1 .08 – – –
Body mass index 1.02 1.0–1.1 .56 – – –
Hypertension 1.13 0.6–2.1 .69 – – –
Coronary artery disease 1.48 0.8–2.8 0.24 – – –
.1 PVC morphology 1.72 0.9–3.3 .10 – – –
Ventricular bigeminy 0.72 0.4–1.4 .30 – – –
PVC coupling interval SD 15.2 0.9–258.3 .06 – – –
NSVT 5 nonsustained ventricular tachycardia; SD 5 standard deviation. Other abbreviations as in Tables 1 and 2.
*Using minimum 24-h burden over the 14-d monitoring period.

considerable daily fluctuation in PVC burden, with minimum
daily burden being 7.3% 6 6.2% and maximum daily burden
being 17.9% 6 8.0%. During the monitoring period, 70
patients (34.0%) had both a 24-hour period with a PVC
burden of ,10% and a PVC burden of .20% over different
24-hour periods (Figure 1). The mean PVC coupling interval
for the dominant morphology was 547 6 85 ms, with little
variability in coupling interval observed (coupling interval
standard deviation 11 6 10 ms).
A univariate analysis was performed to assess different
measures of PVC burden as predictors of adverse LV re-
modeling (LVEF ,45% or left ventricular end-diastolic
volume index .75 mL/m2), as shown in Table 2. Since
we had 14-day patch monitors, we initially analyzed the
predictive value of several measures of PVC burden. The
minimum PVC burden on any day of the 14-day patch
monitor was the strongest predictor of adverse remodeling
(OR 1.07; P 5 .009) as compared with daily maximum
day 1 burden (simulating a standard 24-hour Holter
monitor) or overall mean PVC burden. A minimum daily
PVC burden of .20% yielded the strongest predictive value
of adverse remodeling (OR 2.52; P 5 .008). Table 3 lists the
unadjusted and adjusted ORs for a range of clinical and
ECG/patch-derived risk factors for adverse LV remodeling.
The strongest independent risk factor following multivariate
analysis were presence of NSVT (OR 5.3), longer PVC
coupling interval .500 ms (OR 4.7), PVC burden (OR
4.4 for .20%; OR 3.5 for 10%–20%), and superiorly
directed PVC axis (OR 2.7). The ABC-VT score was
derived on the basis of these multivariate predictors as
shown in using log(OR): 1 point for superior axis, 2 points
for PVC burden 10%–20%, or 3 points for burden .20%, 4
points for coupling interval .500 ms, and 4 points for the
presence of NSVT (Figure 2).
We sought to validate the utility of this risk score in 2
cohorts. Cohort 1 comprised a healthy subgroup of patients
from the derivation cohort (PVC burden .5%) with LVEF
.45% at baseline. Time 5 0 was the date of the index patch
monitor between 2012 and 2017, and all patients were fol-
lowed up until October 2019. Follow-up data were available
for 134 patients with a mean follow-up of 1199 6 638 days.
ABC-VT scores between 0 and 4 were classified as “low
risk” (77 patients [57%]), scores between 5 and 8 as “inter-
mediate risk” (44 patients [33%]), and scores between 9
and 12 as “high risk” (13 patients [10%]). The mean
ABC-VT score was 4.2 6 3.2.
An adverse event, as defined by a composite of absolute
LVEF decline by 10%, heart failure hospitalization, or cardio-
vascular mortality, occurred in 13 patients. The ABC-VT
score was associated with a higher incidence of adverse
events at follow-up (hazard ratio 1.43; 95% confidence inter-
val [CI] 1.19–1.73; P , .001). All 13 patients with events had
an ABC-VT score of 5–11 (mean 8.0 6 1.6 vs 3.8 6 3.1 for
those without adverse events; P , .001). The adverse events
observed were as follows: an absolute LVEF decrease of
10% (9 patients), heart failure hospitalization (3 patients),
and sudden death (1 patient). Time to development of adverse
events by ABC-VT score (stratified into 3 groups on the basis
of low [0–4], intermediate [5–8], or high [9–12] score) is
shown in Figure 3. Positive components of the risk score
observed were VT (13 of 13), coupling interval .500 ms
(10 of 13), superior axis (6 of 13), and PVC burden .10%
(3 of 13). Repeat transthoracic echocardiogram was per-
formed 3.0 6 1.7 years from baseline transthoracic echocar-
diogram with an average absolute change in LVEF of 22.7%
6 7.8%. There was a trend toward a greater decline in LVEF
at follow-up in those with ABC-VT score 5 than in those
with score ,5 (24.3 6 8.6 vs 21.1 6 6.9; P 5 .07). For
1070 Heart Rhythm, Vol 17, No 7, July 2020

Figure 2 ABC-VT risk score (maximum 12).

those with .10% absolute decline in LVEF at follow-up, the
time to echocardiogram was 859 6 535 days, while the time
to the most recent echocardiogram was 1053 6 605 days for
the entire cohort.
We then evaluated the ABC-VT score in an independent
validation cohort of 559 patients from the Korean PVC reg-
istry (cohort 2). This cohort had a mean age of 56 6 17
years, comprised 55% women, had a mean PVC burden of
19.1% 6 10.1%, and had a baseline LVEF of 63% 6 4%.
Baseline characteristics are listed in Online Supplemental
Table 1. The mean ABC-VT score was 4.3 6 2.8. Nineteen
patients developed adverse events over 1474 6 1236 days of
follow-up. The ABC-VT score ranged from 2 to 11 in those
with adverse events, and Figure 4 demonstrates events by

Figure 3 Freedom from adverse events (composite of cardiovascular mortality, absolute left ventricular ejection fraction [LVEF] decline by 10%, or heart
failure hospitalization) over 3.3 6 1.8 years (follow-up data from the original derivation cohort with baseline LVEF .45% and premature ventricular contraction
burden .5%).
Voskoboinik et al ABC-VT Risk Score for Frequent PVCs
Figure 4 Freedom from adverse events (composite of cardiovascular mortality, absolute left ventricular ejection fraction [LVEF] decline by 10%, or heart
failure hospitalization) over 4.0 6 3.4 years (follow-up data from the Korean validation cohort with baseline LVEF .45% and premature ventricular contraction
burden .5%).
low, intermediate, and high ABC-VT scores. A higher ABC-
VT score was associated with a higher risk of adverse events
at follow-up in this cohort (hazard ratio 1.22; 95% CI 1.05–
1.42; P 5 .01). A summary of methods, study design, and
key findings is shown in Online Supplemental Figure 1.
Discussion
The key findings of our study are as follows:
1. Minimum daily PVC burden on a 14-day patch monitor
was more strongly associated with adverse LV remodel-
ing than was daily mean, daily maximum, or 24-hour
PVC burden (simulating a standard Holter).
2. Independent predictors of adverse LV remodeling in
patients with frequent PVCs included superior PVC
axis, minimum PVC burden .10%, coupling interval
.500 ms, and presence of NSVT, which formed the
ABC-VT risk score.
1071
3. In patients with frequent PVCs and preserved LV func-
tion, the ABC-VT risk score predicted future adverse
events with reasonable diagnostic accuracy, with score
2 identifying low-risk patients.
Patients presented with frequent PVCs and reduced LV
function or congestive heart failure have a class I indication
for suppression of PVCs with catheter ablation.13 However,
many patients present with frequent PVCs and preserved
ventricular function. The optimal management in these
patients is unclear. In a seminal study by Bogun and col-
leagues,2 some patients with frequent PVCs had an
associated cardiomyopathy, yet many with high PVC burden
had normal LV function. Therefore, current recommenda-
tions for patients with frequent asymptomatic PVCs are to
pursue watchful waiting, with repeat monitoring and echo-
cardiography at regular intervals to allow the early identifica-
tion of those patients who require therapy.14 This may cause
patient concern and require repeat testing over many years
1072
Figure 5 Examples of “low” vs “high” risk premature ventricular complexes in 2 separate patients based on the ABC-VT score. NSVT 5 nonsustained ven-
tricular tachycardia.
that adds significant cost to the health care system. In addi-
tion, some patients may be lost to follow-up or experience
sudden death with the development of undetected cardiomy-
opathy.15 The ABC-VT risk score is a simple score that, if
validated prospectively, may allow the identification and
early treatment of patients at risk of developing future cardio-
myopathy.
The majority of idiopathic PVCs in the absence of struc-
tural heart disease originate from the left or right ventricular
outflow tract,8 resulting in an inferior axis. Although some
idiopathic PVCs also originate from the papillary muscles,
moderator band, or fascicles, yielding a superior axis, we
found that a superior axis was associated with adverse LV re-
modeling and worse prognosis. In a study of 45 patients with
.10% PVC burden and preserved LVEF followed for 6
months without intervention, non–outflow tract location
Heart Rhythm, Vol 17, No 7, July 2020
was the strongest multivariate predictor of decline in systolic
function (OR 14; 95% CI 1.6–126.84).16 These findings may
relate to early structural changes in the non–outflow tract
regions of the right or left ventricles, greater dyssynchrony
from non–outflow tract sites located further from the
septum,17 or adverse hemodynamic profile from PVCs of api-
cal or inferior origin. In studies comparing right ventricular
apical vs outflow tract pacing lead location (superior vs infe-
rior axis), outflow tract positions have been associated with
less dyssynchrony, improved systolic function, and lower
Brain Natriuretic Peptide (BNP) levels.18 In a recent study
examining patients with frequent PVCs, Muser et al19 identi-
fied PVCs that were not “left bundle branch block/inferior
axis” in addition to age, male sex, family history, unex-
plained syncope, multifocal PVCs, and fibrosis on cardiac
magnetic resonance imaging as predictors of future
Voskoboinik et al ABC-VT Risk Score for Frequent PVCs
malignant arrhythmias. Our end point also includes future
deterioration in LVEF and heart failure hospitalization to
further aid risk stratification and uses a simple, easy-to-use
risk score that can be applied in the office setting on the basis
of the ECG and Holter recording.19
PVC burden has consistently been shown to be the stron-
gest predictor of PVC-induced cardiomyopathy, with the
burden required ranging from 10% to 24%.2 We found a sig-
nificant day-by-day variability in burden over the 14-day
monitoring period, with over a third of patients registering
a mean PVC burden of both ,10% and .20% over separate
24-hour periods. Earlier studies have drawn attention to the
increasing yield of 14-day monitoring, with only 53% of pa-
tients reaching the 10% PVC burden threshold doing so on
day 1 in 1 study20 and 25% of patients having a .5.5-fold
difference between minimum and maximum 24-hour burden
in another series. Awareness of these fluctuations is impor-
tant if clinicians are to solely use 24-hour monitoring for de-
cision making. Surprisingly, the mean PVC burden was a
relatively weak univariate predictor of adverse remodeling
in this series (OR 1.06), arguing that PVC burden alone is
insufficient for risk stratification.
Short-coupled PVCs are more likely to trigger polymor-
phic VT/ventricular fibrillation and adversely affect LV
filling profile and stroke volume.21 However, the impact of
PVC coupling interval on structural remodeling has not
been extensively studied. In a canine model of acutely intro-
duced PVCs, longer PVC coupling intervals were associated
with more pronounced dyssynchrony and reduced LV filling
time for the next sinus beat, which may initiate reflex sympa-
thetic activity and renin-angiotensin-aldosterone system acti-
vation.22 In human studies, longer coupling interval has been
identified as a univariate predictor of LV dysfunction23,24 in
some studies but shorter coupling interval25 or variable
coupling interval23 has been predictive in other studies. In
our cohort, longer coupling interval was a strong predictor
of adverse LV remodeling. This may also relate to a greater
degree of dyssynchronous LV contraction or more pro-
nounced cellular calcium overload at longer coupling inter-
vals. Earlier studies have identified an association between
variability in coupling interval and cardiac arrhythmic
events.26 In our series, there was a signal toward more
adverse remodeling with variable PVC coupling interval
(“coupling interval standard deviation” univariate OR 15.2;
P 5 .06), although statistical significance was not reached.
Figure 5 demonstrates an example of a “high” vs “low”
risk PVC based on the ABC-VT score.
Clinical implications
In patients presenting with frequent PVCs, the presence of a
low ABC-VT risk score appears to portend a good prognosis
and is associated with a low medium-term risk of clinical
deterioration. This may represent a group of patients who
may be managed conservatively. By contrast, patients with
high scores may require closer follow-up and may benefit
from arrhythmia suppression. Catheter ablation is an effec-
1073
tive treatment of PVC-induced cardiomyopathy, with suc-
cessful ablation resulting in marked LVEF improvement27
and/or recovery of LV function28 over time in the over-
whelming majority of patients. As such, the ABC-VT score
may have a future role in identifying “high risk” patients
who may benefit from earlier ablation.
Limitations
Because of the retrospective nature of this study, it is unclear
whether the predictors of adverse LV remodeling identified
are contributory to a reversible PVC-induced cardiomyopa-
thy or reflect early and/or progressive structural heart disease.
As such, the ABC-VT score may simply identify poor prog-
nostic factors associated with PVCs portending a worse
outcome regardless of arrhythmia suppression. Nevertheless,
a low ABC-VT score may identify a group of patients for
which a more conservative approach is reasonable. Measure-
ment of PVC burden by 24-hour Holter in the Korean cohort
(rather than 2-week patch recording) resulted in a lower
detection rate of NSVT and hence lower overall risk scores
in this group. A third validation cohort with 2-week patch
data was not available for this study. Larger prospective
studies are required to further validate this risk score and
determine the impact of PVC suppression on long-term out-
comes.
Conclusion
The ABC-VT score is associated with adverse LV remodel-
ing in patients with frequent PVCs and appears to predict
future clinical deterioration in independent retrospective co-
horts. Larger prospective studies are required to further vali-
date this score as a risk stratification tool for PVCs.
Appendix
Supplementary data
Supplementary data associated with this article can be found
in the online version at https://doi.org/10.1016/j.hrthm.2020.
02.020.
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