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\begin{document}

\title{Insight of Electrocardiographic and Electrophysiological Parameters on
The Left Ventricular Function in Patients with Ventricular Arrhythmia
from Left Ventricular Summit}



\author[1]{Chin-Yu Lin}%
\author[1]{Ming-Jen Kuo}%
\author[1]{Yenn-Jiang Lin}%
\author[1]{Shih-Lin Chang}%
\author[1]{Li-Wei Lo}%
\author[1]{Yu-Feng Hu}%
\author[1]{Fa-Po Chung}%
\author[1]{Ta-Chuan Tuan}%
\author[1]{Tze-Fan Chao}%
\author[1]{Jonan Liao}%
\author[1]{Ting-Yung Chang}%
\author[1]{Ling Kuo}%
\author[1]{Cheng-I Wu}%
\author[1]{Chih-Min Liu}%
\author[1]{Shin-Huei Liu}%
\author[1]{Shih-Ann Chen}%
\affil[1]{Taipei Veterans General Hospital}%


\vspace{-1em}



  
  \date{May 14, 2024}


\begingroup
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\selectlanguage{english}
\begin{abstract}
\textbf{Introduction:} Ventricular arrhythmia (VA) from the left
ventricular summit (LVS) is a common origin of VA, which resulting LV
dysfunction in some patients. However, the predictors of LV
cardiomyopathy were not well-elucidated. The present study sought to
investigate the risk factor of LV cardiomyopathy and the outcome in
patients with LVS VA \textbf{Methods:} Between 2013 and 2018, a total of
139 patients (60.7\% men; mean age 53.2 \selectlanguage{ngerman}± 13.9 years-old) underwent
catheter ablation for LVS VA from two centers. Detailed patient
demographics, electrocardiograms, electrophysiological characteristics,
and clinical outcomes were extracted for analysis. LV cardiomyopathy was
defined as LV ejection fraction (LVEF) \textless{}50\%.
\textbf{Results:} Acute procedural success was achieved in 92.8 \% of
patients. There were 40 patients (28.8\%) with LV cardiomyopathy, and
the mean LVEF improved from 37.5 ± 9.3\% to 48.5 ± 10.2\% after ablation
( \emph{p} \textless{} 0.001). After multivariate analysis, the
independent predictors of LV dysfunction were wider QRS duration of the
VA (odds ratio {[}OR{]}1.02; 95\% confidence interval {[}CI{]}:
1.00-1.04; \emph{p} = 0.046) and the absolute earliest activation time
discrepancy (AEAD) between epicardium and endocardium (OR 1.05; 95\%
confidence interval CI: 1.00-1.09; \emph{p} = 0.048). After ablation,
the LV function was completely recovered in 20 patients (50\%). The
predictors for irreclaimable LV function included wider PVC QRS duration
(OR 1.09; 95\% CI: 1.02-1.17; \emph{p} = 0.012) and poorer LVEF (OR
0.85; 95\% CI: 0.74-0.97; \emph{p} = 0.020). \textbf{Conclusion:} In
patients with VA from LVS, PVC QRS duration and AEAD predicted the
deteriorating LV systolic function. Catheter ablation could reverse the
LV remodeling. Narrower QRS duration and better LVEF predicted a better
recovery of LV function after ablation.%
\end{abstract}\selectlanguage{ngerman}%



\sloppy


\textbf{Insight of Electrocardiographic and Electrophysiological
Parameters on The Left Ventricular Function in Patients with Ventricular
Arrhythmia from Left Ventricular Summit}

Ming-Jen Kuo, MD\textsuperscript{1,2,3*}, Chin-Yu Lin, MD,
PhD\textsuperscript{1,2*}, Yenn-Jiang Lin, MD, PhD\textsuperscript{1,2},
Shih-Lin Chang, MD, PhD\textsuperscript{1,2}, Li-Wei Lo, MD,
PhD\textsuperscript{1,2}, Yu-Feng Hu, MD, PhD\textsuperscript{1,2},
Fa-Po Chung, MD, PhD\textsuperscript{1,2}, Ta-Chuan Tuan,
MD\textsuperscript{1,2}, Tze-Fan Chao, MD, PhD\textsuperscript{1,2},
Jo-Nan Liao, MD, PhD\textsuperscript{1,2}, Ting-Yung Chang,
MD\textsuperscript{1,2}, Ling Kuo, MD\textsuperscript{1,2}, Cheng-I Wu,
MD\textsuperscript{1,2}, Chih-Min Liu, MD\textsuperscript{1,2},
Shin-Huei Liu, MD\textsuperscript{1,2}, Shih-Ann Chen,
MD\textsuperscript{1,2,3}

\textsuperscript{1}Division of Cardiology, Department of Medicine,
Taipei Veterans General Hospital, Taipei, Taiwan

\textsuperscript{2}Institute of Clinical Medicine and Cardiovascular
Research Institute, National Yang-Ming Chiao-Tung University, Taipei,
Taiwan

\textsuperscript{3} Cardiovascular Center, Taichung Veterans General
Hospital, Taichung, Taiwan

* The first two authors contributed equally to this work.

\textbf{Brief running title: Predictor of LV dysfunction in patients
with LVS VA}

\textbf{Total word count of the manuscript: 3173}

\textbf{Disclosures} : None for all authors

\textbf{Address for Correspondence}\selectlanguage{english}
\begin{longtable}[]{@{}ll@{}}
\toprule
Yenn-Jiang Lin, MD, PhD Division of Cardiology Taipei Veterans General
Hospital 201, Sec.2, Shih-Pai Rd, Taipei, Taiwan Tel: 886-2-7735-3832
Fax: 886-2-2872-4082 E-mail: linyennjiang@gmail.com &\tabularnewline
\bottomrule
\end{longtable}

\textbf{Abstract}

\textbf{Introduction:} Ventricular arrhythmia (VA) from the left
ventricular summit (LVS) is a common origin of VA, which resulting LV
dysfunction in some patients. However, the predictors of LV
cardiomyopathy were not well-elucidated. The present study sought to
investigate the risk factor of LV cardiomyopathy and the outcome in
patients with LVS VA

\textbf{Methods:} Between 2013 and 2018, a total of 139 patients (60.7\%
men; mean age 53.2 \selectlanguage{ngerman}± 13.9 years-old) underwent catheter ablation for LVS
VA from two centers. Detailed patient demographics, electrocardiograms,
electrophysiological characteristics, and clinical outcomes were
extracted for analysis. LV cardiomyopathy was defined as LV ejection
fraction (LVEF) \textless{}50\%.

\textbf{Results:} Acute procedural success was achieved in 92.8 \% of
patients. There were 40 patients (28.8\%) with LV cardiomyopathy, and
the mean LVEF improved from 37.5 ± 9.3\% to 48.5 ± 10.2\% after ablation
(\emph{p} \textless{} 0.001). After multivariate analysis, the
independent predictors of LV dysfunction were wider QRS duration of the
VA (odds ratio {[}OR{]}1.02; 95\% confidence interval {[}CI{]}:
1.00-1.04; \emph{p} = 0.046) and the absolute earliest activation time
discrepancy (AEAD) between epicardium and endocardium (OR 1.05; 95\%
confidence interval CI: 1.00-1.09; \emph{p} = 0.048). After ablation,
the LV function was completely recovered in 20 patients (50\%). The
predictors for irreclaimable LV function included wider PVC QRS duration
(OR 1.09; 95\% CI: 1.02-1.17; \emph{p} = 0.012) and poorer LVEF (OR
0.85; 95\% CI: 0.74-0.97; \emph{p} = 0.020).

\textbf{Conclusion:} In patients with VA from LVS, PVC QRS duration and
AEAD predicted the deteriorating LV systolic function. Catheter ablation
could reverse the LV remodeling. Narrower QRS duration and better LVEF
predicted a better recovery of LV function after ablation.

\textbf{Keywords:} Ablation; Left ventricular summit; Left ventricular
function; QRS duration; Ventricular arrhythmia; absolute earliest
activation time discrepancy

\textbf{Introduction}

Premature ventricular complex (PVC) is a common ventricular arrhythmia
(VA). PVCs can cause various symptoms often regarded as
benign\textsuperscript{1, 2}, but also can lead to
cardiomyopathy\textsuperscript{3, 4}. PVC-induced cardiomyopathies are
characterized by deterioration of left ventricular (LV) function, which
can be reversed after the elimination of PVCs \textsuperscript{3-5}.
Several parameters have been proposed to predict PVC-induced
cardiomyopathy, including the PVC burden \textsuperscript{6, 7}, PVC QRS
duration\textsuperscript{8-10}, origin of PVC \textsuperscript{8}, PVC
coupling interval \textsuperscript{11}, symptoms, duration
\textsuperscript{12}, and presence of non-sustained ventricular
tachycardia (VT) or sustained VT \textsuperscript{8}. However, except
for the PVC burden, the prediction values of these parameters were
inconsistent. These parameters remained debated mainly, which could be
due to the heterogeneous PVC origin and the non-uniform underlying
cardiac disease.

PVCs originating from epicardium have been reported as a risk factor for
PVC-induced cardiomyopathy \textsuperscript{9, 13}. The left ventricular
summit (LVS) is the highest portion of the LV epicardium and is an
important anatomic area harboring arrhythmogenic foci responsible for
VA\textsuperscript{14}. VAs arising from LVS frequently required
multiple approach from bother epicardium and endocardial adjacent
area\textsuperscript{15}. There was no previous studies systemically
investigated the incidence, risk factors, and reversibility of LV
dysfunction with successful ablation.

The present study aims to determine the various factors associated with
LV dysfunction induced by VA originating from LVS.

\textbf{Methods}

\textbf{2.1 Study population}

The retrospective study included 139 patients with VAs originating from
the LVS who underwent electrophysiological study and three-dimensional
mapping and ablation at two large centers (Taipei Veterans General
Hospital and Cheng-Hsin Hospital, Taipei, Taiwan) between 2013 and 2019.
The study complied with the Declaration of Helsinki, and each
institutional review board approved the protocol. Data on the baseline
demographic characteristics of the patient's left ventricular ejection
fraction (LVEF), PVC burden, medical therapy, electrocardiographic (ECG)
characteristics, use of multisite ablation, procedural details,
administration of anti-arrhythmic drugs (AADs) before and after
ablation, mapping parameters, and ablation outcomes were collected. The
patients were divided into two groups: the patient with LV dysfunction
(Group 1, LVEF less than 50\%) and the patient with preserved LVEF
(Group 2, LVEF \selectlanguage{english}[?] 50\%) \textsuperscript{16}. The routinely performed
coronary angiography excluded ischemic heart disease before ablation,
and significant structural heart disease was ruled out by
echocardiography.

\textbf{2.2 Assessment of LV function}

Two-dimensional echocardiography was performed before catheter ablation
and then at 3 \textasciitilde{} 6 months after the procedure.
Echocardiograms were performed by experienced ultrasonographers. A
standard imaging protocol was used based on apical 4-chamber views
according to the recommendations of the American Society of
Echocardiography Two independent observers analyzed
echocardiograms.\textsuperscript{17} Three cycles were measured for each
assessment, avoiding post-ectopic beats, and the average volumes were
obtained.

\textbf{2.3 ECG analysis of the PVC morphology and definition of the ECG
criteria}

With standard 12-lead ECG electrode placement, sinus rhythm (SR) and PVC
ECG morphologies were measured on the BARD recording system before
ablation, with the recordings displayed at 100 mm/s. PVC morphology was
defined as right bundle branch block pattern (RBBB) if QRS was positive
in lead V1 or left bundle branch block pattern (LBBB) for negative QRS
in V1. The following measurements were also assessed manually of the
first beat of PVC on the surface ECG by two independent observers: (1)
coupling interval (CI); (2) QRS duration (QRSd); (3) intrinsicoid
deflection time (IDT); (4) Pseudo-delta wave (PdW); (5) maximum
deflection index (MDI); (6) Q-wave ratio in leads aVL and
aVR\textsuperscript{18}.

\textbf{CI}

The CI was measured from the beginning of an SR QRS complex to the
beginning of the PVC.

\textbf{PVC QRSd}

The PVC QRS duration (ms) was defined as the interval measured from the
earliest ventricular activation to offset the QRS complex in the
precordial leads.

\textbf{IDT}

IDT was defined as the interval measured from the earliest ventricular
activation to the peak of the R wave in V2 \textsuperscript{19}.

\textbf{PdW}

The PdW was defined as the interval from the earliest ventricular
activation to the onset of the earliest fast deflection in any
precordial lead \textsuperscript{19}.

\textbf{MDI}

MDI was defined as the interval measured from the earliest ventricular
activation to the peak of the largest amplitude deflection in each
precordial lead (taking the lead with the shortest time) divided by the
QRSd \textsuperscript{20}.

\textbf{Electrophysiology study, mapping, and ablation}

The details of the procedure protocol have been described in our
previous study \textsuperscript{21}. All VAs originated from the LVS by
the definition that the earliest activation site within the LVS (great
cardiac vein/anterior interventricular vein {[}GCV/AIV{]} or epicardium)
based on fluoroscopy and electroanatomic mapping. The absolute earliest
activation time discrepancy (AEAD) was defined as the absolute value of
the difference in the earliest activation times (EAT) preceding the VA
which was obtained from the epicardial (epicardium or GCV/AIV) and
endocardial LVS (AEAD {[}ms{]}
=\selectlanguage{english}|EAT\textsubscript{epi}-EAT\textsubscript{endo}\selectlanguage{english}|) \textsuperscript{22}.
Example cases of VAs from LVS with the AEAD measurement was shown
in\textbf{Figure 1} .

For sustained VTs, acute procedural success was defined as
noninducibility of clinical sustained VT after ablation. For patients
who underwent nonsustained VT/PVC ablation, acute procedural success was
defined as complete elimination, and noninducibility of frequent PVCs
previously observed during the procedure \textsuperscript{21}.

\textbf{Follow up}

The absence of VA recurrences was assessed by 24-hour Holter monitoring
and surface ECG during follow-up. VT recurrences were defined by the
presence of sustained VTs, nonsustained VTs using 24- hour Holter
monitoring and surface ECG and PVCs \textgreater{} 1000/day assessed by
24-hour Holter monitoring \textsuperscript{21}. In addition, the
assessment of the LVEF by echocardiography was repeated 3 to 6 months
after ablation. LV systolic function recovery after ablation was defined
as LVEF \textless{} 50\% before ablation and normalization of LVEF or
LVEF improved at least 15\% after ablation\textsuperscript{12, 23}.

\textbf{Statistical analysis}

Data are expressed as the mean +- standard deviation for normally
distributed continuous variables and proportions for categorical
variables. The continuous variables were analyzed using a two-tailed t
test. Discrete variables were compared using a \selectlanguage{greek}χ\selectlanguage{english}2 test or Fisher's exact
test The association between the selected parameters and PVC-induced
cardiomyopathy was studied by a univariate logistic regression analysis.
The variables selected for testing in the multivariate analysis for a
logistic regression model were those with a P value \textless{} 0.05 in
the univariate models. The differences in the LVEF before and after the
ablation were compared by Student's \emph{t} test. The worst LVEF before
ablation was compared to those after ablation. All statistical
significances were set at a P value \textless{} 0.05, and all
statistical analyses were carried out using SPSS 22.0 software (IBM
Corporation, Armonk, NY).

\textbf{Results}

\textbf{Study population}

As in \textbf{Table 1} , a total of 139 patients with drug-refractory
PVC referred to our institute for ablation were analyzed (40 in group 1
and 99 in group 2). The characteristics of the PVCs during the 24-hour
Holter monitoring were documented, with the mean PVC burden over 24 hour
was 20.6 \selectlanguage{ngerman}± 11.6\%, and 18.0\% of patients with sustained VT and 30.2\%
of those with non-sustained VT. The mean LVEF was 52.4 ± 11.2\%. LV
dysfunction (LVEF\textless{}50\%), defined by echocardiography before
the ablation, was identified in 40 patients (28.8\%). The origin of the
PVC was confirmed to be in the LV summit, with the earliest site in the
epicardium and/or GCV/AIV.

\textbf{Baseline patient and PVC characteristics}

The comparison of the clinical characteristics of patients with (group
1) and without LV dysfunction (group 2) is summarized in \textbf{Table
2} . The mean LVEF in group 1 was 37.5 ± 9.3\% and 58.4 ± 4.1\% in group
2. Compared to patients in group 2, there were more male (80.0\% vs.
58.6\%; \emph{P} = 0.019), documented sustained VT (30.0\%
vs.13.1\%;\emph{P} = 0.027), RBBB pattern of the VA (53.4\% vs. 33.5\%;
\emph{P} = 0.006), longer CI (510.5 ± 66.4 ms vs.483.7 ± 58.8 ms;
\emph{P} = 0.021), wider QRS duration (163.7 ± 28.0 ms vs. 147.2 ± 20.4
ms;\emph{P} = 0.001), and larger AEAD (12.0 ± 9.1 vs. 16.3 ± 8.2 ms; P=
0.012). There was no significant difference in underlying disease,
clinical presentation, baseline medical therapy, PVC burden, or the
successful ablation site.

\textbf{Characteristics associated with the development of LV
dysfunction}

In univariate analysis, as in \textbf{Table 3} , sex, presence of
sustained VT, PVC morphology with RBBB pattern, CI, AEAD, and PVC QRS
duration were associated with an increased risk of LV dysfunction. In
multivariate analysis, only PVC QRS duration and AEAD were independently
associated with the development of LV dysfunction.

\textbf{Ablation outcome and changes in the LV function before and after
the ablation}

The overall acute success rate of the index ablation was 92.8\%. The
successful ablation site was most in the ASV (35.3\%), followed by
GCV/AIV (30.9\%), subvalvular (20.9\%), and epicardium (12.9\%).

The changes in the PVC burden and the corresponding LVEF before and
after ablation of the LV summit PVCs are shown in \textbf{Figure 2} . In
patients with and without LV dysfunction, the PVC burden after the
ablation was significantly decreased than that before the ablation. In
group 2 patients, the LVEF before (58.4 ± 5.0\%) and after (58.4 ±
5.0\%) the ablation was similar (\emph{P} = 0.865). In contrast, the
LVEF significantly improved after ablation in the group 1 patients
(post-LVEF vs. before-LVEF: 48.5 ± 10.2\% vs. 37.5 ± 9.3\%;
\emph{P}\textless{} 0.001).

During a mean follow-up period of 27.6 ± 18.4 months, 26 (18.7\%)
patients had recurrences with a mean duration of 9.1 ± 5.8 months after
the index procedure. Of these 26 patients with recurrence, 22 patients
(84.6\%) had the same PVC morphology as the PVC morphology during the
index procedures, and the other four patients (15.4\%) had recurrences
with different PVC morphology. Compared with group 2, there was a higher
recurrence rate in patients in group 1 (group 1 vs. group 2: 32.5\% vs.
13.1\%; \emph{P} = 0.015). Although there was PVC recurrence during
follow-up, the PVC burden decreased significantly (4.8 ± 7.4\%) compared
to the PVC burden before the index procedure (17.6 ± 8.8\%;
\emph{P}\textless{} 0.001), and the LVEF also improved significantly
(post-LVEF vs. before-LVEF: 53.8 ± 11.8\% vs. 48.2 ± 14.6\%; \emph{P} =
0.037). For group 1 patients, despite PVC recurrences, the PVC burden
significantly decreased (2.2 ± 3.7\% vs.14.5 ± 7.9\%; \emph{P}
\textless{} 0.001) and there were significant improvements for LVEF
after the index procedures (post-LVEF vs. before-LVEF:47.5 ± 13.0\%
vs.35.9 ± 8.7\%; \emph{P} = 0.015).

For 26 patients with PVC recurrences, 11 patients (42.3\%) received
repeat procedures (9 patients with the same PVC morphology and 2
patients with different morphology as the PVC morphology during the
index procedures). Of these 11 patients, 2 patients were in group 1 and
the other 9 patients were in group 2. For these 2 patients in group 1,
both had LV function recovery after the index procedure (one patient
with LVEF improved from 27\% to 42\%, and the other LVEF improved from
25\% to 43\%), and the LV function were similar after the repeat
procedures (LVEF was 45\% in both patients after the repeat procedures).

\textbf{Determinants associated without LV function recovery after
ablation}

Of 40 patients with LV dysfunction (group 1), 20 patients (50.0\%) did
not recover LV function after ablation. As in \textbf{Supplemental Table
I} , of these 20 patients without recovery, there were poorer LVEF at
baseline (34.3 ± 7.3\% vs.40.7 ± 10.1\%; \emph{P} = 0.027), longer PVC
QRS duration (178.3 ± 23.1 ms vs.149.0 ± 24.9 ms; \emph{P} \textless{}
0.001), and with more PVC recurrences after ablation than patients with
LV function recovery (50.0\% vs.15.0\%; \emph{P} = 0.041).

After multivariate analysis \textbf{(Supplement Table II)} , QRS
duration of the PVC and baseline LVEF before the index procedure was
independently predictive for irreclaimable LV function after ablation.

\textbf{Discussion}

\textbf{Main findings}

This is the first study to systematically evaluate the risk factors in
developing LV dysfunction in patients with LV summit VA. In the present
study, we found that:(1) The incidence of LV dysfunction with VA
originated from LVS was 28.8\%; (2) PVC QRS duration and AEAD were
independent predictors of LV dysfunction; (3) After ablation, the LV
systolic function could be improved in patients with LVS VA, and (4) PVC
QRS duration and baseline LVEF before ablation were two predictors for
patients with LV function recovery after ablation.

\textbf{Prevalence and incidence of LV dysfunction in patients with LVS
VA}

The prevalence of PVC-induced cardiomyopathy has been reported at 7\%
among patients with a PVC burden of more than 10\% \textsuperscript{24};
however, it is likely underestimated \textsuperscript{4}. Clinical
studies have reported a diagnosis of PVC-induced cardiomyopathy from 9\%
to 30\% of patients referred for ablation of PVC \textsuperscript{6, 23,
25-27}. Nevertheless, most of the previous studies were heterogeneous on
PVC origin, and Yamada et al. reported that PVC-induced cardiomyopathy
in 19.2\% of patients referred for ablation of PVC originated from
RVOT\textsuperscript{16}. In our study, with all 139 patients, the PVC
originated from LV summit referred for ablation, LV dysfunction was
recognized as 28.8\%.

\textbf{Prediction of LV dysfunction in patients with LVS VA}

Most patients with PVC-induced cardiomyopathy have very frequent PVCs;
however, the PVC burden alone does not reliably predict whether
cardiomyopathy will be induced. Baman et al. demonstrated a PVC burden
of 24\% best predicted those with and without
cardiomyopathy\textsuperscript{6}. Reported cutoff numbers vary from
16\% to 26\%\textsuperscript{6, 7, 24}; however, PVC-induced
cardiomyopathy has been reported in patients with a PVC burden of only
4\% \textsuperscript{28}, and normal heart function is often seen in
patients with a high PVC burden. Similarly, in the present study with
PVC originating from LV summit, the mean PVC burden before ablation was
20.6\%, and it was not associated with PVC-induced cardiomyopathy. LV
dysfunction could be found as low as 5\% of PVC burden, and normal LV
function could be noted in PVC burden as high as 55\% in this large
cohort. The result means that patients' characteristics and PVC features
play more critical roles in the pathophysiology of PVC-induced
cardiomyopathy than PVC burden.

Patients with more prolonged exposure to PVCs or an asymptomatic status
have a higher risk of developing PVC-induced cardiomyopathy in
asymptomatic status \textsuperscript{12}. Patients without symptoms may
have a higher probability of prolonged exposure to PVCs before they are
disclosed. Of the 139 patients in our study population, only 2 (1.4\%)
presented without symptoms, and both had normal LV systolic function.
Because most patients had symptoms, we could not conclude the
association between asymptomatic status and PVC-induced cardiomyopathy
in patients with VA originated from LVS.

PVC QRS duration, with a cut-ff level of \textgreater{}150ms best
separated patients with and without PVC induced cardiomyopathy, reported
by Yokokawa et al \textsuperscript{9}. QRS duration was still be found
to be the predisposing factor for LV dysfunction from the present
study\textsuperscript{9}. The result was in line with previous studies
with PVCs originating from various locations throughout both ventricles.
The proposed mechanisms included ventricular dyssynchrony,
asymmetrically increased wall thickness, and work overload in the late
activated regions, all contributing to further myocardium
remodeling\textsuperscript{4}.

As previously mentioned, most studies focusing on PVC-induced
cardiomyopathy were heterogeneous on PVC origin; however, there were
some reports demonstrated that an epicardial origin was independently
associated with PVC-induced cardiomyopathy \textsuperscript{9, 13, 26}.

Epicardial PVCs are shown to have longer QRS duration than other
PVCs\textsuperscript{9}, maybe due to the paucity of Purkinje fibers in
the epicardium. The initial part of the wavefront progresses slowly
through the myocardial wall until reaching the Purkinje system at the
subendocardium. This slow transmural activation is reflected as the slow
onset of the QRS on the surface electrocardiogram
\textsuperscript{29}and prolonged transmural activation by measuring the
AEAD {[}epi-endo{]}. To the best of our knowledge, this is the first
study to demonstrate the relationship between PVC-induced cardiomyopathy
and AEAD {[}epi-endo{]}, a novel parameter associated with LV
dysfunction in patients with LVS VA, which reflects the depth of
intramural foci. The longer AEAD {[}epi-endo{]} might reflect
superficial epicardial foci, resulting in a longer activation time
difference between epicardial and endocardial exit \textsuperscript{22}.
Although we enrolled all patients with VA originating from LVS, the
wider QRS and larger AEAD {[}epi-endo{]} might indicate VA foci close to
the epicardial surface, causing a long transmural activation time and LV
dyssynchrony.

\textbf{Catheter ablation of LVS VA and the induced LV dysfunction}

Catheter ablation of PVCs has been reported to have an acute success
rate of 80\%-94\%, with a complication rate of up to
5.6\%\textsuperscript{30-32}. However, the outcomes for catheter
ablation of LVS VAs were diverse and the success rate was lower than the
outcomes for PVC ablation originated other than LVS, ranging from 22\%
to 100\% for acute procedural success and from 23\% to 100\% for freedom
from VA recurrences \textsuperscript{14, 18, 33, 34}. In the present
study, ablation of LVS VAs was effective, with a high acute success rate
(92.8\%). Also, in patients with LV dysfunction, the decreased LVEF
improved from 37.5 ± 9.3\% to 48.5 ± 10.2\% (\emph{P} \textless{}
0.001), indicating the reversible phenomenon of PVC-induced
cardiomyopathy, which was comparable to previous studies showing that
after successful ablation of the PVCs originated from various locations,
there was a mean improvement of LVEF from 10\%-15\% \textsuperscript{13,
26, 31, 35, 36}.

In the present study, 50\% of patients recovered LV systolic function.
For patients without recovery, we found that longer VA QRS duration and
poorer LVEF before ablation were two independent factors in predicting
irreclaimable LV dysfunction. Our study was in accordance with previous
study \textsuperscript{37}. Combining with the poor LVEF as another
prediction, the results echoed our postulation that patients with longer
PVC QRS duration may have more severe and irreversible underlying LV
substrate abnormalities, which was an indicator rather than a cause for
LV cardiomyopathy.

\textbf{Clinical Implications}

LVS has been demonstrated to be an essential anatomic focus for the
origin of VA. According to the present study, the incidence of LV
dysfunction in patients with frequent VA from LVS PVC is high (28.8\%).
A significant improvement in LV systolic function in patients with LVS
VA-induced cardiomyopathy could be achieved after successful ablation.
The discrepancy of activation (between endocardium and epicardium) and
the QRSd were the only predictors for LV dysfunction; hence, patients
with longer QRS duration should be advocated for an earlier intervention
to eliminate the VA.

\textbf{Study limitations}

There were several limitations for the present study. First, the present
results were obtained from relatively small study samples and
retrospective in nature, besides, no control group was included in the
present study. The prospective, randomized study with large sample size
to validate the results is mandated. Second, we did not collect cardiac
magnetic resonance (CMR) data, and therefore, myocardial fibrosis before
the ablation could not be analyzed and limiting us to detect significant
CMR predictors of the development of PVC induced cardiomyopathy. Third,
the VA duration was proved to be a predictor for VA induced
cardiomyopathy \textsuperscript{12}, and which was not collected in the
present study.

\textbf{Conclusion}

In patients with VA originating from LVS, LV dysfunction could be
reversed by catheter ablation. VA QRS duration and the AEAD were the
only predictors of LV dysfunction. The VA QRS duration and the baseline
LVEF could predict the reversibility of LV dysfunction after catheter
ablation.

\textbf{Funding Sources:} The present work was supported by grants from
the Taipei Veterans General Hospital (V110B-042, VN111-05, V111C-128,
C19-027, C13-092), the Ministry of Science and Technology
(109-2314-B-075-076-MY3,
109-2314-B-010-058-MY2,110-2314-B-A49A-541-MY3,111-2314-B-075 -007
-MY3~), and the Research Foundation of Cardiovascular Medicine
(110-02-006).

\textbf{Disclosure:} There is no financial interest or relationship to
disclose

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\textbf{Figure legend}

\textbf{Figure 1.} The activation map of two patients with symptomatic
premature ventricular complex originated from the left ventricle summit.
Figure (A) and (B) showed one patient with premature ventricular complex
(PVC) with QRS duration 142ms. Figure (B) showed the earliest activation
site was localized over the distal great cardiac vein (GCV) (EAT: 29 ms
pre-QRS), while in Figure (A) the earliest activation within the left
ventricle (LV) was located at LV summit region over left ventricular
outflow tract (LVOT), just opposite to the EAT of the distal GCV (EAT:
22 ms pre-QRS). The AEAD was 7 (=\selectlanguage{english}|29-22\selectlanguage{english}|) ms. The patient pre-procedural
LV ejection fraction (LVEF) was 55\%, and it was 61\% after the
procedure. Figure (C) and (D) showed another patient with PVC with QRS
duration 174ms. Figure (D) showed the earliest activation site was
originated from the distal GCV (EAT: 35 ms pre-QRS), while in Figure
(D), the earliest activation site within the LV endocardium was located
near LV summit region over LVOT (EAT: 20ms pre-QRS). The AEAD was 15
(=\selectlanguage{english}|35-20\selectlanguage{english}|) ms. The patient pre-procedural LVEF was 36\%, and it became
43\% after the ablation procedure. LV, left ventricle; RVOT, right
ventricular outflow tract.

\textbf{Figure 2.} The changes of the PVC burden and the LVEF before and
after ablation. Panel A showed the changes of the PVC burden before and
after the ablation in those with or without PVC induced cardiomyopathy.
Panel B showed changes of LVEF before and after ablation in those with
or without PVC induced cardiomyopathy. PVC, premature ventricular
complex; LVEF, left ventricular ejection fraction; CMP, cardiomyopathy.
*\emph{P} \textless{} 0.001

\textbf{Figure 1.}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image1/image1}

\end{center}
\end{figure}

\textbf{Figure 2.}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/image2/image2}

\end{center}
\end{figure}\selectlanguage{english}
\begin{longtable}[]{@{}ll@{}}
\toprule
\textbf{Table 1. Patient Characteristics (N = 139)} & \textbf{Table 1.
Patient Characteristics (N = 139)}\tabularnewline
Variables & Variables\tabularnewline
Age, years old & 53.2 \selectlanguage{ngerman}±1 3.9\tabularnewline
Male (n, \%) & 90 (64.7\%)\tabularnewline
Hypertension (n, \%) & 23 (16.5\%)\tabularnewline
Diabetes (n, \%) & 11 (7.9\%)\tabularnewline
Symptom of Palpitation (n, \%) & 137 (98.6\%)\tabularnewline
Symptom of Syncope (n, \%) & 17 (12.2\%)\tabularnewline
Medication before ablation &\tabularnewline
Beta blocker or CCB only (n, \%) & 54 (38.8\%)\tabularnewline
Class I AAD (n, \%) & 49 (35.3\%)\tabularnewline
Amiodarone (n, \%) & 31 (22.3\%)\tabularnewline
Clinical VA pattern &\tabularnewline
Presence of Sustained VT (n, \%) & 25 (18.0\%)\tabularnewline
Presence of Non-Sustained VT (n, \%) & 42 (30.2\%)\tabularnewline
PVC burden (pre-ablation) (beats/day) & 21924 \selectlanguage{ngerman}± 12349\tabularnewline
PVC burden (pre-ablation) (\%)* & 20.6 \selectlanguage{ngerman}± 11.6\tabularnewline
LVEF (pre-ablation) (\%)* & 52.4 \selectlanguage{ngerman}± 11.2\tabularnewline
PVC induced cardiomyopathy (n, \%) & 40 (28.8\%)\tabularnewline
VA morphology &\tabularnewline
RBBB morphology (n, \%) & 46 (33.1\%)\tabularnewline
Coupling interval & 491.4 \selectlanguage{ngerman}± 62.1\tabularnewline
QRSd, ms & 151.9 \selectlanguage{ngerman}± 24.0\tabularnewline
IDT, ms & 59.8 \selectlanguage{ngerman}± 21.2\tabularnewline
PdW, ms & 57.8 \selectlanguage{ngerman}± 20.6\tabularnewline
Q-wave aVL/aVR ratio & 1.40 \selectlanguage{ngerman}± 0.46\tabularnewline
MDI & 0.47 \selectlanguage{ngerman}± 0.13\tabularnewline
Earliest activation before VA (ms) & -35.6 \selectlanguage{ngerman}± 14.3\tabularnewline
Multiple site ablation requirement (n, \%) & 78 (56.1\%)\tabularnewline
Successful ablation site (n, \%) &\tabularnewline
ASV & 49 (35.3\%)\tabularnewline
Subvalvular & 29 (20.9\%)\tabularnewline
GCV/AIV & 43 (30.9\%)\tabularnewline
Epicardium & 18 (12.9\%)\tabularnewline
Acute procedural success (n, \%) & 129 (92.8\%)\tabularnewline
AAD, anti-arrhythmic drug; AIV, anterior Interventricular vein; ASV,
aortic sinus~of Valsalva; CCB, calcium channel blocker; GCV, great
cardiac vein; IDT, intrinsicoid deflection time; LVEF, left ventricular
ejection fraction; MDI, maximum deflection index; VA, ventricular
arrhythmia; PdW, pseudo-delta wave; VT, ventricular tachycardia; PVC,
premature ventricular complex; QRSd, QRS duration; RBBB, right bundle
branch block; & AAD, anti-arrhythmic drug; AIV, anterior
Interventricular vein; ASV, aortic sinus~of Valsalva; CCB, calcium
channel blocker; GCV, great cardiac vein; IDT, intrinsicoid deflection
time; LVEF, left ventricular ejection fraction; MDI, maximum deflection
index; VA, ventricular arrhythmia; PdW, pseudo-delta wave; VT,
ventricular tachycardia; PVC, premature ventricular complex; QRSd, QRS
duration; RBBB, right bundle branch block;\tabularnewline
\bottomrule
\end{longtable}

\textbf{Table 2.} Comparisons of the factors between patients with or
without cardiomyopathy\selectlanguage{english}
\begin{longtable}[]{@{}llll@{}}
\toprule
\begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
\textbf{Normal LV function} \textbf{(N = 99)}\strut
\end{minipage} & \begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
\textbf{LV cardiomyopathy} \textbf{(N = 40)}\strut
\end{minipage} & \begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
\emph{P} \textbf{value}\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Age (y/o)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
52.3 \selectlanguage{ngerman}± 13.5\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
55.3 \selectlanguage{ngerman}± 15.0\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.254\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Male (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
58 (58.6\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
32 (80.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.019\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Hypertension (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
17 (17.2\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
6 (15.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Diabetes (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
8 (8.1\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
3 (7.5\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Symptom of Palpitation (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
97 (98.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
40 (100.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Symptom of Syncope (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
10 (10.1\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
7 (17.5\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.257\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Medication before ablation\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Beta blocker or CCB only (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
39 (39.4\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
15 (37.5\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Class I AAD (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
36 (36.4\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
13 (32.5\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.700\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Amiodarone (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
19 (19.2\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
12 (30.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.182\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Clinical VA pattern\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Presence of Sustained VT (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
13 (13.1\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
12 (30.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.027\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Presence of Non-Sustained VT (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
33 (33.3\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
9 (22.5\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.228\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
PVC burden (pre-ablation) (beats/day)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
22467 \selectlanguage{ngerman}± 12419\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
20597 \selectlanguage{ngerman}± 12307\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.510\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
PVC burden (pre-ablation) (\%)*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
20.9 \selectlanguage{ngerman}± 11.6\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
20.0 \selectlanguage{ngerman}± 11.6\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.631\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Ejection fraction (pre-ablation) (\%)*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
58.4 \selectlanguage{ngerman}± 4.1\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
37.5 \selectlanguage{ngerman}± 9.3\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\textless{}0.001\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
VA morphology\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
RBBB morphology (n,\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
27 (27.3\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
19 (47.5\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.029\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Coupling interval\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
483.7 \selectlanguage{ngerman}± 58.8\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
510.5 \selectlanguage{ngerman}± 66.4\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.021\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
QRSd, ms\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
147.2 \selectlanguage{ngerman}± 20.4\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
163.7 \selectlanguage{ngerman}± 28.0\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.001\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
IDT, ms\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
58.2 \selectlanguage{ngerman}± 20.8\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
63.8 \selectlanguage{ngerman}± 21.9\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.155\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
PdW, ms\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
56.9 \selectlanguage{ngerman}± 20.7\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
59.9 \selectlanguage{ngerman}± 20.4\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.438\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Q-wave aVL/aVR ratio\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.36 \selectlanguage{ngerman}± 0.48\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.49 \selectlanguage{ngerman}± 0.39\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.130\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
MDI\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.47 \selectlanguage{ngerman}± 0.13\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.46 \selectlanguage{ngerman}± 0.13\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.617\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Successful ablation site (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
ASV\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
38 (38.4\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
11 (27.5\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.246\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Subvalvular\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
21 (21.2\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
8 (20.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
GCV/AIV\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
28 (28.3\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
15 (37.5\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.315\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Epicardium\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
12 (12.1\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
6 (15.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.781\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
AEAD\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
12.0 \selectlanguage{ngerman}± 9.1\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
16.3 \selectlanguage{ngerman}± 8.2\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.012\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Multiple site ablation requirement (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
56 (56.6\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
22 (55.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

\textbf{Table 3.} Multivariate analysis for predictors of cardiomyopathy
in the patients with VA from LV summit.\selectlanguage{english}
\begin{longtable}[]{@{}lllllll@{}}
\toprule
& Univariate analysis & Univariate analysis & Univariate analysis &
Multivariate analysis & Multivariate analysis & Multivariate
analysis\tabularnewline
& Crude OR & 95\% CI & P value & Adjusted OR & 95\% CI & P
value\tabularnewline
Age & 1.02 & 0.99-1.04 & 0.253 & & &\tabularnewline
Male & 2.83 & 1.18-6.76 & 0.019 & 1.72 & 0.66-4.46 &
0.266\tabularnewline
Hypertension & 0.85 & 0.31-2.34 & 0.755 & & &\tabularnewline
Diabetes & 0.92 & 0.23-3.67 & 0.909 & & &\tabularnewline
Symptom of syncope & 1.89 & 0.66-5.37 & 0.233 & & &\tabularnewline
Clinical VA pattern & & & & & &\tabularnewline
Presence of sustained VT & 2.84 & 01.16-6.93 & 0.022 & 1.60 & 0.63-4.59
& 0.290\tabularnewline
Presence of NSVT & 0.58 & 0.25-1.36 & 0.211 & & &\tabularnewline
PVC burden (pre-ablation), \%* & 0.99 & 0.95-1.03 & 0.627 & &
&\tabularnewline
VA morphology* & & & & & &\tabularnewline
RBBB morphology & 2.41 & 1.13-5.17 & 0.023 & 1.48 & 0.63-3.49 &
0.368\tabularnewline
Coupling interval & 1.01 & 1.00-1.01 & 0.026 & 1.00 & 1.00-1.01 &
0.223\tabularnewline
QRSd, ms & 1.03 & 1.01-1.05 & \textless{}0.001 & 1.02 & 1.00-1.04 &
0.046\tabularnewline
IDT, ms & 1.01 & 0.99-1.03 & 0.156 & & &\tabularnewline
PdW, ms & 1.01 & 0.99-1.03 & 0.435 & & &\tabularnewline
Q aVL/aVR ratio & 1.88 & 0.83-4.25 & 0.132 & & &\tabularnewline
MDI & 0.48 & 0.03-8.61 & 0.614 & & &\tabularnewline
Successful ablation site & Successful ablation site & Successful
ablation site & Successful ablation site & Successful ablation site &
Successful ablation site & Successful ablation site\tabularnewline
ASV & 0.61 & 0.27-1.36 & 0.226 & & &\tabularnewline
Subvalvular & 0.93 & 0.37-2.31 & 0.874 & & &\tabularnewline
GCV/AIV & 1.52 & 0.70-3.30 & 0.289 & & &\tabularnewline
Epicardium & 1.28 & 0.45-3.68 & 0.648 & & &\tabularnewline
AEAD & 1.04 & 1.00-1.08 & 0.039 & 1.05 & 1.00-1.10 &
0.048\tabularnewline
Multiple site ablation requirement & 0.94 & 0.45-1.97 & 0.866 & &
&\tabularnewline
AAD, anti-arrhythmic drug; AEAD, absolute earliest activation time
discrepancy; AIV, anterior Interventricular vein; ASV, aortic sinus~of
Valsalva; CCB, calcium channel blocker; GCV, great cardiac vein; IDT,
intrinsicoid deflection time; LVEF, left ventricular ejection fraction;
MDI, maximum deflection index; VA, ventricular arrhythmia; PdW,
pseudo-delta wave; VT, ventricular tachycardia; PVC, premature
ventricular complex; QRSd, QRS duration; RBBB, right bundle branch
block; & AAD, anti-arrhythmic drug; AEAD, absolute earliest activation
time discrepancy; AIV, anterior Interventricular vein; ASV, aortic
sinus~of Valsalva; CCB, calcium channel blocker; GCV, great cardiac
vein; IDT, intrinsicoid deflection time; LVEF, left ventricular ejection
fraction; MDI, maximum deflection index; VA, ventricular arrhythmia;
PdW, pseudo-delta wave; VT, ventricular tachycardia; PVC, premature
ventricular complex; QRSd, QRS duration; RBBB, right bundle branch
block; & AAD, anti-arrhythmic drug; AEAD, absolute earliest activation
time discrepancy; AIV, anterior Interventricular vein; ASV, aortic
sinus~of Valsalva; CCB, calcium channel blocker; GCV, great cardiac
vein; IDT, intrinsicoid deflection time; LVEF, left ventricular ejection
fraction; MDI, maximum deflection index; VA, ventricular arrhythmia;
PdW, pseudo-delta wave; VT, ventricular tachycardia; PVC, premature
ventricular complex; QRSd, QRS duration; RBBB, right bundle branch
block; & AAD, anti-arrhythmic drug; AEAD, absolute earliest activation
time discrepancy; AIV, anterior Interventricular vein; ASV, aortic
sinus~of Valsalva; CCB, calcium channel blocker; GCV, great cardiac
vein; IDT, intrinsicoid deflection time; LVEF, left ventricular ejection
fraction; MDI, maximum deflection index; VA, ventricular arrhythmia;
PdW, pseudo-delta wave; VT, ventricular tachycardia; PVC, premature
ventricular complex; QRSd, QRS duration; RBBB, right bundle branch
block; & AAD, anti-arrhythmic drug; AEAD, absolute earliest activation
time discrepancy; AIV, anterior Interventricular vein; ASV, aortic
sinus~of Valsalva; CCB, calcium channel blocker; GCV, great cardiac
vein; IDT, intrinsicoid deflection time; LVEF, left ventricular ejection
fraction; MDI, maximum deflection index; VA, ventricular arrhythmia;
PdW, pseudo-delta wave; VT, ventricular tachycardia; PVC, premature
ventricular complex; QRSd, QRS duration; RBBB, right bundle branch
block; & AAD, anti-arrhythmic drug; AEAD, absolute earliest activation
time discrepancy; AIV, anterior Interventricular vein; ASV, aortic
sinus~of Valsalva; CCB, calcium channel blocker; GCV, great cardiac
vein; IDT, intrinsicoid deflection time; LVEF, left ventricular ejection
fraction; MDI, maximum deflection index; VA, ventricular arrhythmia;
PdW, pseudo-delta wave; VT, ventricular tachycardia; PVC, premature
ventricular complex; QRSd, QRS duration; RBBB, right bundle branch
block; & AAD, anti-arrhythmic drug; AEAD, absolute earliest activation
time discrepancy; AIV, anterior Interventricular vein; ASV, aortic
sinus~of Valsalva; CCB, calcium channel blocker; GCV, great cardiac
vein; IDT, intrinsicoid deflection time; LVEF, left ventricular ejection
fraction; MDI, maximum deflection index; VA, ventricular arrhythmia;
PdW, pseudo-delta wave; VT, ventricular tachycardia; PVC, premature
ventricular complex; QRSd, QRS duration; RBBB, right bundle branch
block;\tabularnewline
\bottomrule
\end{longtable}

\textbf{Supplemental Table 1.} Comparisons of factors between LV
function recovery or not in PVC induced cardiomyopathy after RFA.\selectlanguage{english}
\begin{longtable}[]{@{}llll@{}}
\toprule
\begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
\textbf{Without recovery} \textbf{(N = 20)}\strut
\end{minipage} & \begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
\textbf{With recovery} \textbf{(N = 20)}\strut
\end{minipage} & \begin{minipage}[b]{0.24\columnwidth}\raggedright\strut
\emph{P} \textbf{value}\strut
\end{minipage}\tabularnewline
\midrule
\endhead
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Age (y/o)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
59.7 \selectlanguage{ngerman}± 14.6\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
50.8 \selectlanguage{ngerman}± 14.3\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.059\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Male (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
18 (90.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
14 (70.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.235\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Hypertension (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
3 (15.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
3 (15.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Diabetes (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
2 (10.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1 (5.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Medication before ablation\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Beta blocker or CCB only (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
7 (35.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
8 (40.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Class I AAD (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
8 (40.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
5 (25.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.501\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Amiodarone (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
5 (25.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
7 (35.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.731\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Presence of Sustained VT (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
9 (45.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
3 (15.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.082\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Presence of Non-Sustained VT (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
5 (25.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
4 (20.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
PVC burden (pre-ablation) (beats/day)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
21267 \selectlanguage{ngerman}± 10968\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
19760 \selectlanguage{ngerman}± 14266\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.759\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
PVC burden (pre-ablation) (\%)*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
19.5 \selectlanguage{ngerman}± 9.3\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
19.8 \selectlanguage{ngerman}± 14.3\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.948\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Ejection fraction (pre-ablation) (\%)*\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
34.3 \selectlanguage{ngerman}± 7.3\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
40.7 \selectlanguage{ngerman}± 10.1\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.027\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
VA morphology\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
RBBB morphology (n,\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
10 (50.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
9 (45.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Coupling interval\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
522.0 \selectlanguage{ngerman}± 75.6\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
499.0 \selectlanguage{ngerman}± 55.3\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.278\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
QRSd, ms\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
178.3 \selectlanguage{ngerman}± 23.1\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
149.0 \selectlanguage{ngerman}± 24.9\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\textless{}0.001\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
IDT, ms\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
64.7 \selectlanguage{ngerman}± 24.3\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
63.0 \selectlanguage{ngerman}± 19.9\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.815\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
PdW, ms\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
57.4 \selectlanguage{ngerman}± 20.5\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
62.5 \selectlanguage{ngerman}± 20.5\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.432\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Q-wave aVL/aVR ratio\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.55 \selectlanguage{ngerman}± 0.43\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.44 \selectlanguage{ngerman}± 0.36\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.376\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
MDI\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.44 \selectlanguage{ngerman}± 0.13\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.48 \selectlanguage{ngerman}± 0.12\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.271\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Earliest activation before VA (ms)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
-41.2 \selectlanguage{ngerman}± 10.2\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
-40.5 \selectlanguage{ngerman}± 24.2\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.906\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Successful ablation site (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
ASV\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
5 (25.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
6 (30.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Subvalvular\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
6 (30.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
2 (10.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.235\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
GCV/AIV\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
7 (35.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
8 (40.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Epicardium\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
2 (10.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
4 (20.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.661\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Multiple site ablation requirement (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
14 (70.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
8 (40.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.111\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
AEAD\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
16.3\selectlanguage{ngerman}±8.6\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
16.3\selectlanguage{ngerman}±7.9\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.985\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
Acute procedural success (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
18 (90.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
17 (85.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
1.000\strut
\end{minipage}\tabularnewline
\begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
PVC recurrence (n, \%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
10 (50.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
3 (15.0\%)\strut
\end{minipage} & \begin{minipage}[t]{0.22\columnwidth}\raggedright\strut
0.041\strut
\end{minipage}\tabularnewline
\bottomrule
\end{longtable}

AAD, anti-arrhythmic drug; AEAD, absolute earliest activation time
discrepancy; AIV, anterior Interventricular vein; ASV, aortic sinus~of
Valsalva; CCB, calcium channel blocker; GCV, great cardiac vein; IDT,
intrinsicoid deflection time; LVEF, left ventricular ejection fraction;
MDI, maximum deflection index; VA, ventricular arrhythmia; PdW,
pseudo-delta wave; VT, ventricular tachycardia; PVC, premature
ventricular complex; QRSd, QRS duration; RBBB, right bundle branch
block;

\textbf{Supplemental Table 2.} Multivariate Analysis for Predictors of
persistent LV dysfunction after RFA.\selectlanguage{english}
\begin{longtable}[]{@{}lllllll@{}}
\toprule
& Univariate analysis & Univariate analysis & Univariate analysis &
Multivariate analysis & Multivariate analysis & Multivariate
analysis\tabularnewline
& Crude OR & 95\% CI & P value & Adjusted OR & 95\% CI & P
value\tabularnewline
Age & 1.04 & 0.99-1.09 & 0.065 & 1.09 & 0.99-1.20 & 0.090\tabularnewline
Male & 3.86 & 0.67-22.11 & 0.130 & & &\tabularnewline
Hypertension & 1.00 & 0.18-5.67 & 1.000 & & &\tabularnewline
Diabetes & 2.11 & 0.18-25.35 & 0.556 & & &\tabularnewline
Presence of sustained VT & 4.64 & 1.02-21.0 & 0.047 & 14.88 &
0.52-425.67 & 0.115\tabularnewline
Presence of NSVT & 1.33 & 0.30-5.93 & 0.705 & & &\tabularnewline
PVC burden (pre-ablation), \%* & 0.99 & 0.93-1.07 & 0.943 & &
&\tabularnewline
LVEF (pre-ablation) & 0.92 & 0.85-0.99 & 0.036 & 0.85 & 0.74-0.97 &
0.020\tabularnewline
VA morphology* & & & & & &\tabularnewline
RBBB morphology & 1.22 & 0.35-4.24 & 0.752 & & &\tabularnewline
Coupling interval & 1.01 & 0.99-1.02 & 0.280 & & &\tabularnewline
QRSd, ms & 1.05 & 1.02-1.08 & 0.003 & 1.09 & 1.02-1.17 &
0.012\tabularnewline
IDT, ms & 1.00 & 0.98-1.03 & 0.810 & & &\tabularnewline
PdW, ms & 0.99 & 0.96-1.02 & 0.422 & & &\tabularnewline
Q aVL/aVR ratio & 2.13 & 0.41-11.06 & 0.368 & & &\tabularnewline
MDI & 0.50 & 0.01-9.72 & 0.266 & & &\tabularnewline
EAT & 0.99 & 0.96-1.03 & 0.903 & & &\tabularnewline
Successful ablation site & Successful ablation site & Successful
ablation site & Successful ablation site & Successful ablation site &
Successful ablation site & Successful ablation site\tabularnewline
ASV & 0.78 & 0.19-3.13 & 0.724 & & &\tabularnewline
Subvalvular & 3.86 & 0.67-22.11 & 0.130 & & &\tabularnewline
GCV/AIV & 0.81 & 0.22-2.91 & 0.744 & & &\tabularnewline
Epicardium & 0.44 & 0.07-2.76 & 0.384 & & &\tabularnewline
Multiple site ablation requirement & 3.50 & 0.95-12.97 & 0.061 & &
&\tabularnewline
AEAD & 0.999 & 0.926-1.079 & 0.984 & & &\tabularnewline
Acute procedural success & 1.59 & 0.24-10.70 & 0.635 & &
&\tabularnewline
PVC recurrence & 5.67 & 1.25-25.61 & 0.024 & 12.56 & 0.78-202.15 &
0.074\tabularnewline
\bottomrule
\end{longtable}

AAD, anti-arrhythmic drug; AEAD, absolute earliest activation time
discrepancy; AIV, anterior Interventricular vein; ASV, aortic sinus~of
Valsalva; CCB, calcium channel blocker; GCV, great cardiac vein; IDT,
intrinsicoid deflection time; LVEF, left ventricular ejection fraction;
MDI, maximum deflection index; VA, ventricular arrhythmia; PdW,
pseudo-delta wave; VT, ventricular tachycardia; PVC, premature
ventricular complex; QRSd, QRS duration; RBBB, right bundle branch
block;\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-1/Figure-1}

\end{center}
\end{figure}\selectlanguage{english}
\begin{figure}[H]
\begin{center}
\includegraphics[width=0.70\columnwidth]{figures/Figure-2/Figure-2}

\end{center}
\end{figure}

\selectlanguage{english}
\FloatBarrier
\end{document}

