JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY
23, 2017
Listen to this manuscript’s
audio summary by
JACC Editor-in-Chief
Dr. Valentin Fuster.
VOL. 70, NO.
ª 2017 BY THE AMERICAN COLLEGE OF CARDIOLOGY FOUNDATION ISSN 0735-1097/$36.00
PUBLISHED BY ELSEVIER https://doi.org/10.1016/j.jacc.2017.10.030
STATE-OF-THE-ART REVIEW
Catheter Ablation of Ventricular
Tachycardia in Structural Heart Disease
Indications, Strategies, and Outcomes—Part II
Srinivas R. Dukkipati, MD, Jacob S. Koruth, MD, Subbarao Choudry, MD, Marc A. Miller, MD, William Whang, MD,
Vivek Y. Reddy, MD
ABSTRACT
In contrast to ventricular tachycardia (VT) that occurs in the setting of a structurally normal heart, VT that occurs in patients
with structural heart disease carries an elevated risk for sudden cardiac death (SCD), and implantable cardioverter-defibrillators
(ICDs) are the mainstay of therapy. In these individuals, catheter ablation may be used as adjunctive therapy to treat or prevent
repetitive ICD therapies when antiarrhythmic drugs are ineffective or not desired. However, certain patients with frequent
premature ventricular contractions (PVCs) or VT and tachycardiomyopathy should be considered for ablation before ICD
implantation because left ventricular function may improve, consequently decreasing the risk of SCD and obviating the need
for an ICD. The goal of this paper is to review the pathophysiology, mechanism, and management of VT in the setting of
structural heart disease and discuss the evolving role of catheter ablation in decreasing ventricular arrhythmia recurrence.
(J Am Coll Cardiol 2017;70:2924–41) © 2017 by the American College of Cardiology Foundation.
O ver the past 2 decades, improved identifica-
tion of individuals who are at high risk for
sudden cardiac death (SCD) has led to an
increase in the use of implantable cardioverter-
arrhythmias that occur in the setting of structural
heart disease and discuss the role of catheter ablation
and patient populations who are most likely to
benefit from this treatment modality.
defibrillators (ICDs). Consequently, more individuals
survive ventricular tachycardia (VT) or ventricular MECHANISM AND SUBSTRATE FOR VT IN
fibrillation (VF) episodes. This, together with an STRUCTURAL HEART DISEASE
increased understanding of the mechanisms and sub-
strates responsible for ventricular arrhythmias, has POST-MYOCARDIAL INFARCTION. The prototypical,
led to a growth in catheter ablation as a treatment and best understood, substrate for scar-related re-
modality for VT. Catheter ablation is being increas- entrant VT is post-myocardial infarction (MI) VT.
ingly performed as adjunctive therapy to prevent or Following MI, ventricular myocardium can broadly be
reduce ICD therapies when antiarrhythmic drugs are classified as normal, dense scar, or border zone
ineffective or not desired. However, there is often tissue—the latter consisting of interconnected sur-
confusion among practicing physicians regarding in- viving myocardial fibrils interspersed among a bed of
dications, outcomes, and patient populations that electrically inert fibrotic tissue. Together with
are most likely to benefit. In this paper, we review decreased cell-to-cell coupling, partly related to
the mechanisms and substrates for ventricular altered connexin 43 expression, slow and circuitous
From the Helmsley Electrophysiology Center, Department of Cardiology, Icahn School of Medicine at Mount Sinai, New York, New
York. Dr. Dukkipati has received a research grant from Biosense Webster. Dr. Koruth has served as a consultant for Biosense
Webster and Abbott. Dr. Reddy has received research grants from and served as a consultant for Biosense Webster, Boston
Scientific, and Abbott. All other authors have reported that they have no relationships relevant to the contents of this paper to
disclose. Roderick Tung, MD, served as Guest Editor for this paper.
Manuscript received September 25, 2017; revised manuscript received October 11, 2017, accepted October 17, 2017.
JACC VOL. 70, NO. 23, 2017
DECEMBER 12, 2017:2924–41
electrical conduction through the border zone pre-
disposes to re-entrant VT (1–4). Additionally, there
are adaptive and maladaptive changes in cardiac
autonomic innervation that also predispose to VT (5–
8). Sympathetic and parasympathetic efferent inputs
to the convergent local circuit neurons are increased,
whereas afferent inputs from infarcted tissue are
decreased relative to those from the border zone and
normal tissue; this results in a heterogeneity of
autonomic innervation, contributing to the arrhyth-
mogenic substrate (7).
As multiple pathways often exist, numerous circuits
are commonly present and manifest as multiple
inducible VTs during electrophysiological testing (9).
The 12-lead electrocardiogram (ECG) morphology of
each VT depends on the exit of the re-entrant circuit
into the normal myocardium. Although most VT exit
sites are subendocardial, midmyocardial or epicardial
exit sites also exist. Surviving tissue in the border zone
can be identified based on its abnormal conduction
properties and characteristic electrograms (i.e., late
and fractionated potentials) (Figure 1) and is often the
target for ablation.
Although this fundamental understanding of the
pathophysiology of post-MI VT has not changed since
the mid-1990s, recent post-MI mapping studies using
ultra high-resolution mapping technologies have
suggested that patients may have few arrhythmogenic
border zone areas of relatively constrained size (10).
These small, anatomically fixed areas display direc-
tion- and rate-dependent slowing of conduction
velocity related to highly curved activation patterns in
areas of voltage <0.1 mV, and ablation of these rela-
tively small areas resulted in VT termination and
noninducibility. However, the generalizability of this
observation is unknown and requires additional study.
In addition to scar-related re-entry, certain post-MI
patients may present with ventricular arrhythmias
related to the Purkinje system. First described in pa-
tients with idiopathic polymorphic VT or VF, focal
premature ventricular contractions (PVCs) originating
from Purkinje fibers may serve as triggers for these
arrhythmias (11). Similarly, following MI, triggered
activity (due to delayed after depolarizations) from
surviving Purkinje fibers situated along the scar
border may cause focal PVCs that trigger polymorphic
VT/VF (12–15). Additionally, focal VT originating from
the Purkinje system in the setting of acute ischemia
has been attributed to triggered activity and delayed
after depolarizations (16), in contrast to a re-entrant
mechanism that is responsible for monomorphic VT
following remote MI (17). Catheter ablation is possible
for the treatment of these various Purkinje-related
ventricular arrhythmias.
Dukkipati et al. 2925
Catheter Ablation of VT in Structural Heart Disease
Although best described following MI, any ABBREVIATIONS
disease process that predisposes to myocar- AND ACRONYMS
dial scar may cause re-entrant VT. These
ARVC/D = arrhythmogenic
include dilated cardiomyopathy, arrhythmo- right ventricular
genic right ventricular cardiomyopathy/ cardiomyopathy/dysplasia
dysplasia (ARVC/D), hypertrophic cardiomy- CSD = cardiac sympathetic
opathy, cardiac sarcoidosis, Chagas disease, denervation
and surgically repaired congenital heart dis- DAD = delayed after
depolarizations
ease. However, unlike post-MI scar, which has
a predilection for the subendocardium, scar in DCM = dilated cardiomyopathy
these disease states may occur in mid- HCM = hypertrophic
cardiomyopathy
myocardial and epicardial locations. Indeed,
ICD = implantable
epicardial catheter ablation is often required
cardioverter-defibrillator
in these disease states. Although there is an
LAVA = local abnormal
assumption that all scar-related re-entry is ventricular activity
similar, there is a paucity of studies that report
LVAD = left ventricular assist
detailed activation mapping of the re-entrant device
circuit across nonischemic substrates. MI = myocardial infarction
PVC = premature ventricular
DILATED CARDIOMYOPATHY. The ventricular
contraction
myocardium of individuals with dilated car-
SCD = sudden cardiac death
diomyopathy (DCM) is histologically charac-
VF = ventricular fibrillation
terized by multiple regions of patchy
VT = ventricular tachycardia
interstitial and replacement fibrosis, myofiber
disarray, and variable degrees of myocyte hypertrophy
and atrophy (18). Cardiovascular myocardial reso-
nance (CMR) with late gadolinium enhancement
identifies fibrosis in up to 41% and is an important
predictor of sudden cardiac death and VT (19,20). In
early studies, the mechanism of DCM-related VT was
estimated to be scar-related re-entry in 62%, focal
automaticity or triggered activity in 27%, and His-
Purkinje re-entry (bundle branch re-entry VT) in 19%
(21). However, these early studies were skewed by the
exclusion of most patients with hemodynamically
unstable VT; more recent studies suggest that re-entry
is by far the primary VT mechanism in DCM-VT. Unlike
post-MI scar that has a predilection for the sub-
endocardium, scar in DCM may be midmyocardial or
epicardial and most often occurs in the basal ante-
roseptal and inferolateral LV regions (19,20,22–25).
ARRHYTHMOGENIC RIGHT VENTRICULAR
CARDIOMYOPATHY/DYSPLASIA. ARVC/D is charac-
terized by replacement of right ventricular (RV)
myocardium with fibrofatty tissue that begins in
a subepicardial location and progresses toward
the endocardial surface. Although predominantly
involving the RV, left dominant and biventricular
variants also exist (26). Thus, the triangle of
dysplasia, which is classically described as involving
the RV inflow tract, RV outflow tract, and RV apex, is
now thought to include the basal inferior RV, basal
anterior RV, and posterolateral LV; the RV apex is
spared until advanced stages of the disease (27,28).
2926 Dukkipati et al. JACC VOL. 70, NO. 23, 2017

Catheter Ablation of VT in Structural Heart Disease DECEMBER 12, 2017:2924–41

F I G U R E 1 Myocardial Scar and Substrate for Re-Entrant VT

V1

MAP *
Fractionated Potential

V1

MAP
*
Late Potential

V1

Normal
Myocardium
MAP
Border Zone
LAVA
Scar

(Left) Electrical activation from the normal myocardium through border zone tissue is slow and delayed (red arrows). Multiple myocardial
channels are present and can be identified by characteristic electrograms that can be classified as fractionated electrograms (top, asterisk),
late potentials (middle, asterisk), or local abnormal ventricular activity (bottom). In this case, LAVA is best appreciated with ventricular
pacing, which separates the local abnormal electrogram (dashed arrow) from the far-field electrogram with demonstration of local entrance
block to the site with the third complex. These myocardial channels may all serve as potential pathways for different ventricular tachy-
cardias. LAVA ¼ local abnormal ventricular activity; MAP ¼ mapping catheter.

Ventricular arrhythmias, including frequent PVCs
and VT, are the major manifestation of disease and
cause SCD. The PVCs and VT are typically left bundle
branch block morphology and may have an inferior
(similar to idiopathic outflow tract VT) or superior
axis. Sustained VT occurs in approximately one-third
of patients with ARVC/D over 3 years. The vast ma-
jority of episodes are sustained monomorphic VT
(97%) due to scar-related re-entry (29).
aneurysms (0.8% vs. 0.6%/year; p ¼ 0.64), but ven-
tricular arrhythmias occur more frequently (4.7% vs.
0.9%/year; p < 0.001) (33). Nearly 30% of HCM patients
with LV aneurysms and primary prevention ICDs
experience monomorphic VT, and another 3.7% expe-
rience VF during w4.5 years of follow-up (33). The
mechanism of monomorphic VT in these patients is also
scar-related re-entry and is amenable to catheter abla-
tion (32–36).

HYPERTROPHIC CARDIOMYOPATHY CARDIAC SARCOIDOSIS

In high-risk individuals with hypertrophic cardio-
myopathy (HCM) receiving an ICD for either primary or
secondary prevention, the overall rate of ICD inter-
vention is 5.5%/year (primary prevention 3.6%/year;
secondary prevention 10.6%/year) (30). Monomorphic
VT accounts for 38% of episodes (31). Although mono-
morphic VT may occur in any HCM patient with
myocardial scar, the subgroup of patients with LV an-
eurysms seems to be at higher risk (32–36). Mortality
rates are similar in those with and without LV
Sarcoidosis is a systemic inflammatory process result-
ing in noncaseating granulomas. Although most
commonly associated with pulmonary involvement,
myocardial involvement is frequent and is reported to
be present in up to 25% of patients on autopsy (37).
Clinical manifestations are often absent, although
conduction system abnormalities, heart failure,
and ventricular arrhythmias may occur (38). Sarcoid-
osis infiltrates consist of highly differentiated mono-
nuclear phagocytes and CD4þ T cells that initially
JACC VOL. 70, NO. 23, 2017
DECEMBER 12, 2017:2924–41
promote an inflammatory process, and later exert an
anti-inflammatory effect and tissue scarring (39). Due
to progressive inflammation and a complex underlying
substrate, ventricular arrhythmias may have several
mechanisms, including abnormal automaticity, trig-
gered activity, or scar-related re-entry (40). CMR with
18
delayed enhancement and F-fluorodeoxyglucose-
positron emission tomography are useful to define the
extent of myocardial scar and inflammation, respec-
tively. When inflammation is present, the combination
of immunosuppressive therapy and antiarrhythmic
drugs may decrease VT recurrence. However, when
these fail, catheter ablation is feasible (41,42).
CHAGAS CARDIOMYOPATHY. Chagas disease is caused
by the flagellate protozoan parasite Trypanosoma
cruzi and is transmitted by hematophagous tri-
atomine insect vectors. It is endemic to Latin Amer-
ican countries, but is also prevalent in nonendemic
areas due to population migration (43). One-third of
infected individuals will develop chronic symptom-
atic disease, with cardiac involvement being the most
frequent and severe manifestation (44). Chronic
myocarditis affects all cardiac chambers and may
result in conduction system abnormalities, segmental
wall motion abnormalities, diastolic dysfunction, and
LV systolic dysfunction. Wall motion abnormalities,
resulting from myocardial scarring, most frequently
affect the inferolateral and apical LV segments, oc-
casionally culminating in apical aneurysms. Mono-
morphic VT due to scar-related re-entry can arise
from any scar location, but the inferolateral segment
is the most common source, accounting for w80% of
VTs (45). Although endocardial ablation is effective,
recurrence rates are high, likely related to the pres-
ence of epicardial circuits in up to 37% of patients
(46). To eliminate these Chagas-related epicardial VT
circuits, Sosa et al. (47,48) first described the tech-
nique of pericardial mapping using a percutaneous
subxyphoid approach. Long-term success rates of
catheter ablation in Chagas patients are markedly
improved with the incorporation of epicardial map-
ping and ablation (46).
MANAGEMENT
ICDs AND ANTIARRHYTHMIC DRUGS. Numerous
multicenter randomized clinical trials support ICDs
as the principal treatment modality for the primary
and secondary prevention of SCD in patients with
structural heart disease (49–51). Although the mor-
tality benefit has been consistent in patients with
coronary artery disease, the benefit of primary pre-
vention ICDs in nonischemic cardiomyopathy has
recently been questioned. Current guidelines
Dukkipati et al. 2927
Catheter Ablation of VT in Structural Heart Disease
supporting ICD implantation in this population are
largely based on the SCD-HeFT (Sudden Cardiac
Death in Heart Failure Trial), COMPANION (Compar-
ison of Medical Therapy, Pacing, and Defibrillation in
Heart Failure), and DEFINITE (Defibrillators in Non-
Ischemic Cardiomyopathy Treatment Evaluation)
studies, which together demonstrated reduced mor-
tality (52–54). In the more recent DANISH (Danish
Study to Assess the Efficacy of ICDs in Patients with
Non-ischemic Systolic Heart Failure on Mortality),
the primary endpoint of all-cause mortality was
similar between groups randomized to ICD or usual
clinical care (hazard ratio [HR]: 0.87; 95% confidence
interval [CI]: 0.68 to 1.12; p ¼ 0.28) (55). However,
1) there was still a significant reduction of SCD with
the ICD (HR: 0.50; 95% CI: 0.31 to 0.82; p ¼ 0.005);
and 2) a pooled analysis of 6 primary prevention trials
demonstrated a statistically significant 23% risk
reduction in all-cause mortality with the ICD
(HR: 0.77; 95% CI: 0.64 to 0.91) (55,56). Finally,
contemporary studies support programming to a long
VT detection interval and a high VF detection rate to
decrease rates of overall ICD therapy (antitachycardia
pacing and shocks), inappropriate therapy, and
potentially, mortality (57,58).
Beta-blockers, if not contraindicated, are recom-
mended as they decrease mortality following VT/VF
and in patients with heart failure and reduced left
ventricular function (59). They are ineffective as sole
therapy at decreasing VT/VF recurrence, but the
combination of amiodarone and beta-blockers
significantly decreases the rate of recurrent ICD
shocks compared with either sotalol or beta-blockers
alone (60). However, in a meta-analysis, anti-
arrhythmic drugs did not decrease mortality, but
were associated with a 34% reduction in rates of
appropriate ICD therapies and a 70% reduction in
inappropriate ICD therapies (61). The reduction in VT
was largely driven by studies involving amiodarone,
which interestingly, is itself associated with higher
all-cause mortality in ICD recipients. Additionally,
adverse drug reactions related to amiodarone occur in
approximately 30% of patients, requiring alternative
drug therapy or catheter ablation (62).
Despite these limitations, for VT patients with
structural heart disease, the combination of beta-
blocker and amiodarone is the typical drug regimen
for VT/VF suppression. Mexiletine is often added for
breakthrough VT/VF. Other medications such as
sotalol or dofetilide are typically secondary options.
Thus, for patients with recurrent ICD therapies,
antiarrhythmic drugs are useful to decrease VT/VF
recurrence, but do not alter mortality; indeed, amio-
darone may increase mortality.
2928 Dukkipati et al.
Catheter Ablation of VT in Structural Heart Disease
CATHETER ABLATION
INDICATIONS FOR CATHETER ABLATION. For patients
with structural heart disease, catheter ablation as sole
therapy is not indicated for the primary or secondary
prevention of SCD. Rather, it is employed as adjunc-
tive therapy to ICD implantation for secondary pre-
vention when antiarrhythmic drugs are either
ineffective or not desirable. Four multicenter, ran-
domized clinical studies have evaluated the adjunc-
tive role of catheter ablation in addition to ICDs for
the secondary prevention of ventricular arrhythmias.
The SMASH-VT (Substrate Mapping and Ablation in
Sinus Rhythm to Halt Ventricular Tachycardia) study
randomized patients with prior MI presenting with
spontaneous VT/VF to ICD implantation alone or in
combination with catheter ablation (63). Patients
taking class I or III antiarrhythmic drugs were
excluded. Catheter ablation resulted in a 65% reduc-
tion in the rate of appropriate ICD therapy. Similarly,
the VTACH (Ventricular Tachycardia Ablation in
Coronary Heart Disease) study randomized patients
with prior MI, LVEF #50%, and hemodynamically
stable VT to ICD implantation or ICD implantation
and ablation (64). Amiodarone was used in 35% of
patients in each group at the time of randomization.
At w2 years, the primary endpoint of time to first
recurrence of VT or VF was significantly longer with
the ablation group versus control group (median
18.6 months vs. 5.9 months). The freedom from VT/VF
was 47% in the ablation group and 29% in the
control group (HR: 0.61; 95% CI: 0.37 to 0.99;
p ¼ 0.045). In the SMS (Substrate Modification Study),
catheter ablation failed to decrease the primary
endpoint of time to first VT/VF recurrence in post-MI
patients with LVEF #40% and hemodynamically un-
stable VT (65). However, ablation did result in a >50%
reduction in total ICD interventions. Antiarrhythmic
drug (class I or III) use was approximately 30% in both
groups at time of enrollment.
Recently, the VANISH (Ventricular Tachycardia
Ablation versus Escalated Antiarrhythmic Drug Ther-
apy in Ischemic Heart Disease) trial evaluated the
relative roles of catheter ablation versus escalating
antiarrhythmic drug therapy in post-MI ICD patients
with recurrent VT despite receiving class I or III drugs,
a typically encountered clinical situation (62). The
composite primary endpoint of death, VT storm, or
appropriate ICD shock was reduced by 28% with abla-
tion (HR: 0.72; 95% CI: 0.53 to 0.98; p ¼ 0.04). None of
the individual components of the primary endpoint
were significantly different between groups, likely
because of the relatively small sample (n ¼ 259).
JACC VOL. 70, NO. 23, 2017
DECEMBER 12, 2017:2924–41
It should be noted that in these 4 trials, there were
differences in ICD programming and how VT/VF re-
currences were defined that may partially account for
differences in outcomes. Additionally, none of the 4
aforementioned multicenter randomized clinical trials
support catheter ablation for the reduction of
mortality.
In patients with structural heart disease, the 2009
European Heart Rhythm Association and Heart
Rhythm Society Expert Consensus on Catheter
Ablation of Ventricular Arrhythmias recommends
catheter ablation for: 1) patients with sustained
monomorphic VT that recurs despite antiarrhythmic
drugs or when drugs are not tolerated or desired;
2) control of incessant sustained monomorphic VT or
VT storm that is not due to a transient reversible
cause; 3) bundle branch re-entrant or interfascicular
VT; 4) frequent PVCs, nonsustained or sustained VT
in the setting of ventricular dysfunction; and
5) recurrent sustained polymorphic VT and VF that is
refractory to antiarrhythmic therapy and thought to
be secondary to a trigger that is amenable for abla-
tion (66). Additionally, catheter ablation is consid-
ered for sustained monomorphic VT despite therapy
with class I/III antiarrhythmic drugs, as an alterna-
tive to amiodarone in patients with prior MI and
LVEF >30%, and as an alternative to antiarrhythmic
drugs for hemodynamically tolerated sustained
monomorphic VT due to prior MI and LVEF >35%.
The 2014 European Heart Rhythm Association/Heart
Rhythm Society/Asia Pacific Heart Rhythm Society
Expert Consensus on Ventricular Arrhythmias and
the 2015 European Society of Cardiology (ESC)
guidelines for the management of ventricular ar-
rhythmias provide additional and slightly different
recommendations regarding the role of catheter
ablation (67,68). These various recommendations are
consistent with our approach, summarized in the
Central Illustration.
OVERVIEW OF CATHETER ABLATION. C a t h e t e r
a b l a t i o n t e c h n i q u e s . The general approach to cath-
eter ablation of VT involves the characterization of
target VTs, delineation of the arrhythmic substrate,
and radiofrequency ablation of the arrhythmic tissue.
Target VTs include all clinically occurring VTs and
those induced with programmed stimulation. Typi-
cally, programmed ventricular stimulation is per-
formed at 2 drive cycle lengths with up to 3 extrastimuli
delivered at progressively shorter coupling intervals at
2 ventricular locations. When VT is induced, pace-
termination or electrical cardioversion is performed,
and programmed stimulation is continued until the
same VT is repeatedly induced or multiple electrical
JACC VOL. 70, NO. 23, 2017 Dukkipati et al. 2929
DECEMBER 12, 2017:2924–41 Catheter Ablation of VT in Structural Heart Disease

C E N T R A L IL L U ST R A T I O N Role of Catheter Ablation in the Management of Patients With Structural Heart Disease

Structural Heart Disease

Frequent PVCs or NSVT Sustained PMVT or VF

Sustained MMVT
with LV Dysfunction due to PVC Trigger

Incessant
Single Recurrent
VT or VT
Catheter Ablation Episode VT
Storm
Catheter Failure
AADs
Ablation
Failure
Catheter
Ablation
AADs
ICD

Consider AADs ICD

VT Suppression
Normal LV Function on
Reassessment

ICD
Failure
No Yes Catheter
AADs
Ablation
ICD if LVEF ICD Not
≤35% Indicated

Dukkipati, S.R. et al. J Am Coll Cardiol. 2017;70(23):2924–41.

In patients with sustained MMVT and PMVT/VF due to PVC triggers, catheter ablation is typically performed as adjunctive therapy to ICD implantation to reduce
arrhythmia recurrence. However, in patients with PVCs and left ventricular dysfunction, catheter ablation should be considered primary therapy, because ICD
implantation may be avoided if LVEF improves. AAD ¼ antiarrhythmic drugs; ICD ¼ implantable cardioverter-defibrillator; LV ¼ left ventricular; LVEF ¼ left ventricular
ejection fraction; MMVT ¼ monomorphic ventricular tachycardia; NSVT ¼ nonsustained ventricular tachycardia; PMVT ¼ polymorphic ventricular tachycardia;
PVC ¼ premature ventricular contraction; VF ¼ ventricular fibrillation; VT ¼ ventricular tachycardia.

cardioversions are required. For each VT, the 12-lead
ECG morphology, the rate (or cycle length), bundle
branch block morphology, axis, precordial transition,
and the hemodynamic effect are all recorded. This not
only helps localize the VT exit site, but also helps
determine the ablation strategy as described in the
following text.
The myocardial scar is identified using a 3-
dimensional (3D) electroanatomic mapping system
that allows: 1) spatial localization of a mapping cath-
eter; 2) generation of a 3D anatomic representation of
the ventricle that is color-coded based on electrogram
voltage amplitude recorded from the mapping cath-
eter to differentiate normal myocardium from scar or
border zone tissue; and 3) cataloging of myocardial
channels and potential VT circuit isthmus sites
identified on the basis of abnormal electrogram
characteristics, entrainment, or pace mapping.
Normal myocardium is typically characterized by bi-
polar voltage >1.5 mV, dense scar by bipolar
voltage <0.5 mV, and border zone tissue by bipolar
voltage of 0.5 to 1.5 mV (69). As previously described,
myocardial channels responsible for re-entrant VT
reside in the border zone. These channels have
characteristic bipolar electrograms and can be classi-
fied as fractionated electrograms or as late (or iso-
lated) potentials. Fractionated electrograms have
multiple components without an isoelectric segment
and an amplitude #0.5 mV, a duration $133 ms,
and/or an amplitude/duration ratio #0.005. A late or
isolated potential occurs after the QRS complex and is
separated from the ventricular electrogram by an
isoelectric interval of >20 ms (Figure 1) (70,71). Limi-
tations of voltage mapping include variation of
2930 Dukkipati et al.
Catheter Ablation of VT in Structural Heart Disease
bipolar and unipolar amplitudes due to wave front
direction, electrode size and spacing, as well as
annotation of multiple component signals to the
largest peak.
Sites demonstrating late or isolated potentials
correlate with critical portions of the VT circuit
isthmus and are desirable targets for ablation (72,73).
Fractionated and late/isolated potentials may be un-
derappreciated during sinus rhythm and may manifest
only with ventricular pacing. In sinus rhythm, these
electrograms may demonstrate superimposed local
electrical activity and far-field ventricular activity
inscribed during the QRS complex. Ventricular pacing
may cause a delay of the local electrogram and cause
separation from the far-field component. These
abnormal electrograms, together with fractionated
and late/isolated potentials, are broadly classified as
local abnormal ventricular activity (LAVA) and have
also been shown to be desirable ablation targets for VT
(74). However, it should be noted that zones of slow
conduction or deceleration may be more functionally
relevant than the latest activated regions (75).
After VT induction and delineation of
arrhythmic substrate, ablation strategies typically
include a combination of entrainment mapping,
activation mapping, pace mapping, and substrate
modification for VT. Certain sites demonstrating
fractionated electrograms, late/isolated potentials, or
LAVA in sinus rhythm may show diastolic electro-
gram activity during VT. However, not all of these
locations will be critical for maintaining VT; they may
simply represent diastolic activity due to passive
activation (Figure 2). The most reliable method for
determining the relevance of a channel of activation
is to utilize entrainment maneuvers during VT (76). A
detailed description of entrainment is beyond the
scope of this paper; briefly, it involves overdrive
pacing of VT from a site to determine whether that
site is a critical component of the tachycardia circuit
or is a bystander site. Targeting of the sites that fulfill
entrainment criteria for VT circuit isthmus sites has a
high incidence of terminating VT (Figure 3).
Activation mapping involves the identification of
the earliest site of electrical activation in a cardiac
chamber in comparison to an arbitrary reference
electrogram during VT. This information can be color
coded and recorded on a 3D electroanatomic map so
that the earliest site of local electrical activation can
be identified. This is particularly useful for focal VT
that has a single earliest site with centrifugal activa-
tion away from that location. Because electrical ac-
tivity is continuous, activation mapping in re-entrant
VT is not useful to delineate early and late activation;
however, it can be used to identify VT exit sites along
JACC VOL. 70, NO. 23, 2017
DECEMBER 12, 2017:2924–41
the scar border and identification of diastolic corri-
dors during VT. These areas of diastolic activation
may or may not represent critical components of the
VT circuit (isthmus vs. bystander sites) but are often
targeted for ablation.
Entrainment and activation mapping cannot be
performed in the presence of hemodynamically un-
stable VT, which is reported to occur in 69% of pa-
tients with ischemic cardiomyopathy undergoing VT
ablation (9). After scar delineation in sinus rhythm,
pace mapping is a methodology utilized to target
these unstable VTs without requiring VT induction.
This involves pacing along the scar periphery to
match the paced 12-lead ECG morphology with the
clinical VT morphology, thereby identifying the VT
exit sites. Pacing adjacent to the exit site, but further
within the scar, may identify potential VT isthmus
sites, characterized by latency between the pacing
stimulus and the paced QRS (stimulation to QRS in-
terval >80 ms) (72,77,78). Alternatively, substrate
modification of the scar can be performed that targets
all fractionated/late potentials and LAVA.
the The traditional approach to ablation of scar-related
VT has involved using a combination of entrainment/
activation mapping for hemodynamically tolerated
VT and pace mapping and substrate modification for
unstable VT. We previously demonstrated that it is
possible to map otherwise hemodynamically unstable
VT during tachycardia with the use of percutaneous
left ventricular assist devices (LVADs) (79,80). These
devices maintain end-organ perfusion during pro-
longed periods of VT, allowing a longer time for
detailed entrainment/activation mapping, requiring
fewer terminations for hemodynamic instability, and
resulting in more VT terminations with ablation.
However, the observational studies are non-
randomized, and are thus unable to demonstrate
long-term outcome benefits such as mortality reduc-
tion or VT suppression. In our experience, these de-
vices decrease post-procedure heart failure and may
be of potential benefit during VT ablation in patients
with New York Heart Association functional class $III
heart failure, severe LV dysfunction, or electrical
storm, as these types of patients are at high risk for
acute hemodynamic decompensation following abla-
tion (81,82).
Although somewhat more complicated to use,
extracorporeal membrane oxygenation (ECMO) pro-
vides maximal hemodynamic support (>4.5 l/min)
and is of potential benefit when placed preemptively
in high-risk patients undergoing VT ablation or as a
bailout measure when intraprocedural hemodynamic
deterioration occurs (83). In these patients, ECMO
was not only safe, but also allowed prolonged VT
JACC VOL. 70, NO. 23, 2017 Dukkipati et al. 2931
DECEMBER 12, 2017:2924–41 Catheter Ablation of VT in Structural Heart Disease

F I G U R E 2 Myocardial Scar and Mechanism of Re-Entrant VT

A I
Normal
II
Myocardium
III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Border Zone MAP *

Scar

B
Normal
I
Myocardium
II

III
aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Border Zone MAP *

Scar

(A) A VT circuit (red arrow) is dependent upon slow and circuitous electrical activity through border zone tissue during the diastolic period
(orange dashed lines), which are recorded as diastolic electrograms (black asterisk) on the MAP. Locations distal to the VT circuit (orange
asterisks) may also demonstrate diastolic electrograms due to passive activation (orange arrows). Critical locations are identified only with
entrainment and termination of VT with ablation. The QRS morphology of the VT is dependent upon the exit site from border zone tissue to
the normal myocardium (red star). (B) Another VT circuit with a different exit site would demonstrate a different QRS morphology on
electrocardiography. MAP ¼ mapping catheter; VT ¼ ventricular tachycardia.

activation mapping (median 30 min) and a high rate
of VT termination with ablation (81% of patients). In
unstable patients, ECMO can bridge unstable patients
to permanent LVAD or heart transplantation (83).
Bundle branch re-entrant VT typically occurs in
dilated cardiomyopathy but can also be seen in other
diseases with underlying His-Purkinje disease (84).
The rate is often rapid and poorly tolerated hemo-
dynamically. The mechanism is macro–re-entry and
involves both the right and left bundle branches,
ventricular myocardium, and the His bundle. Left
bundle branch block morphology during VT is more
common than a right bundle branch block pattern.
Typically, the retrograde limb is the left bundle
2932 Dukkipati et al. JACC VOL. 70, NO. 23, 2017

Catheter Ablation of VT in Structural Heart Disease DECEMBER 12, 2017:2924–41

F I G U R E 3 Catheter Ablation of Scar-Related VT in a Patient With Prior Inferior Wall Myocardial Infarction

A D
Apex

Septum

MV

Lateral
Apex

INFERIOR LEFT LATERAL/CAUDAL INFERIOR

B C
I I
II II
III III
aVR aVR
aVL aVL
aVF aVF
V1 V1
V2 V2
V3 V3
V4 V4
V5 V5
V6 V6
Termination
MAP
* * MAP

(A) Electroanatomic bipolar voltage maps of the left ventricle in the inferior (left) and left lateral/caudal (right) views are shown. Normal ventricular myocardium is
purple (>1.5 mV), and dense scar is red (<0.5 mV). Late potentials (black points) and fractionated electrograms (pink points) are seen throughout the inferior wall
scar. (B) At a location within the scar (yellow circles in A), the MAP demonstrates a late potential (left asterisk) during a ventricular pacing and a diastolic electrogram
(right asterisk) during VT. Entrainment during VT identified this location as an isthmus site for the VT circuit. (C) Ablation at this location resulted in VT termination in
8.4 s. (D) In addition to this location, all identified myocardial channels were ablated (red points) either during a paced rhythm or during hemodynamically stable VT.
Abbreviations as in Figure 2.

branch and the antegrade limb is the right bundle
branch. A His electrogram precedes every QRS com-
plex, and any variation in the VT cycle length is pre-
ceded by a variation in the His-His timing. Typically,
catheter ablation of the right bundle is curative;
however, in those with an underlying left bundle
branch block in sinus rhythm, the risk of complete
heart block is increased, and ablation with elimina-
tion of left bundle branch retrograde conduction is
preferable.
The technique for catheter ablation of polymorphic
VT/VF due to PVC triggers and of PVCs resulting in left
ventricular dysfunction in patients with structural
heart disease is similar to that in patients with struc-
turally normal hearts, and was reviewed in part I of this
series.
Epicardial a b l a t i o n . Although most VT circuits
in post-MI patients are subendocardial, a third of
patients may require epicardial ablation for mid-
myocardial or subepicardial circuits (85). Further-
more, as previously mentioned, epicardial mapping is
useful in DCM VT, particularly in ARVC/D and Chagas
disease, due to preponderance of midmyocardial and
subepicardial scar. The epicardial space is accessed
using a percutaneous subxyphoid puncture approach
in those patients without prior cardiac surgery, and
JACC VOL. 70, NO. 23, 2017 Dukkipati et al. 2933
DECEMBER 12, 2017:2924–41 Catheter Ablation of VT in Structural Heart Disease

F I G U R E 4 Bipolar Voltage Maps of the RV Endocardium and Epicardium in a Patient With ARVC/D and Recurrent VT

A B

PV

RV ENDOCARDIAL EPICARDIAL

(A) The bipolar voltage map of the RV endocardium (anterior posterior view) shows a large area of scar (red area) on the inferior and free
walls. (B) There is also a large area of scar seen on the RV epicardial surface. Radiofrequency ablation (red points) was required on the
endocardial and epicardial surfaces of the RV to successfully abolish the multiple VTs that were induced. All late potentials (black points) and
fractionated potentials (pink points) were also targeted. ARVC/D ¼ arrhythmogenic right ventricular cardiomyopathy/dysplasia;
PV ¼ pulmonary valve; RV ¼ right ventricular; VT ¼ ventricular tachycardia.

by a surgical subxyphoid or limited anterior thora-
cotomy approach in most patients with prior surgery
(47,86,87).
Pre-procedural imaging is useful in identifying in-
dividuals that may benefit from an
approach. The presence of midmyocardial or sub-
epicardial scar on CMR identifies patients that are
likely to require epicardial mapping for successful
abolition of VT (25). The use of pre-procedural CMR
has been shown to be independently associated with
improved procedural success and the composite
endpoint of VT recurrence, heart transplantation, or
death in DCM patients undergoing VT ablation (88).
Patients that should be considered for epicardial
mapping include those with: a failed prior ablation,
VT unrelated to coronary artery disease (i.e., DCM,
ARVC/D, HCM, and Chagas cardiomyopathy, where
there is a higher likelihood of subepicardial scar), a
CMR suggesting midmyocardial or epicardial scar, or
an ECG suggestive of an epicardial exit (Figures 4
and 5). A number of ECG criteria have been identi-
fied as supporting an epicardial VT exit (89–91).
Among these, the easiest to recognize is a slow
upstroke/downstroke of the initial part of the QRS
complex during VT (a pseudo-delta wave). Although
these criteria are widely used, their discriminatory
power in the setting of myocardial scar has been
questioned (92,93).
OUTCOMES OF CATHETER ABLATION. The results of
catheter ablation in post-MI patients are reasonable,
epicardial with 1-year recurrence rates between 23% and 49%,
and with many patients remaining on antiarrhythmic
drugs (94–96). These results were obtained with
mostly traditional VT mapping techniques, such as
entrainment/activation mapping of hemodynamically
stable VT and pace mapping, and limited substrate
ablation for poorly tolerated VT. Recently, alternate
predominantly substrate-based ablation strategies
targeting all of the arrhythmogenic myocardium
(fractionated/late potentials and LAVA) in sinus
rhythm have been evaluated (74,85,97–99). These
strategies have yielded higher success rates when all
identifiable myocardial channels were targeted. In
the VISTA (Ablation of Clinical Ventricular Tachy-
cardia Versus Addition of Substrate Ablation on the
Long Term Success Rate of VT Ablation) trial (100),
ischemic cardiomyopathy patients with hemody-
namically tolerated VT were randomized to target
clinical VTs using entrainment, activation, and pace
mapping versus an extensive substrate-based abla-
tion strategy targeting all abnormal electrograms
within the scar. The primary endpoint of VT
2934 Dukkipati et al. JACC VOL. 70, NO. 23, 2017

Catheter Ablation of VT in Structural Heart Disease DECEMBER 12, 2017:2924–41

F I G U R E 5 Catheter Ablation of VT in HCM With Midcavitary Obstruction and Apical Aneurysm

A B

C I
II
III
aVR
aVL
aVF
V1
V2
V3
V4
V5

V6
VT Termination
9.0 s
MAP d

MAP p

(A) A left ventriculogram of an HCM patient presenting with monomorphic VT is shown in a right anterior oblique view. During systole, a large
apical aneurysm with a small neck is seen (dashed line). (B) Bipolar voltage maps of the LV endocardium and epicardium of another HCM
patient with an apical aneurysm are shown. This patient had recurrent VT despite prior endocardial ablation. The LV endocardial map shows an
infarcted apical aneurysm (red) with otherwise normal tissue at the base (purple). The epicardial map (mesh) also demonstrated apical scar
and highlights the thickness of the myocardium, particularly at the neck of the aneurysm and base. Catheter ablation at the epicardial
surface (arrow) terminated VT. The areas with late and fractionated potentials (black and pink points, respectively) in sinus rhythm were all
targeted with ablation (red points). (C) VT terminated in 9.0 s during epicardial ablation (arrow in B). HCM ¼ hypertrophic cardiomyopathy;
LV ¼ left ventricular; other abbreviations as in Figure 2.

recurrence at 12 months was 48.3% in the clinical VT
ablation group and 15.5% in the substrate ablation
group (log-rank p < 0.001). Substrate ablation was
associated with a 67% lower risk of VT recurrence
compared with clinical VT ablation (HR: 0.33; 95% CI:
0.13 to 0.81; p ¼ 0.014). There were no differences in
mortality between the groups.
The results of catheter ablation in dilated cardio-
myopathy are generally worse than in ischemic car-
diomyopathy, due to a higher preponderance of
intramural substrate and infrequent
ablation targets (i.e., fractionated and late potentials)
(22,95,101–106). With the addition of epicardial map-
ping to the ablation strategy for ARVC/D patients, the
success rates of catheter ablation have markedly
improved (107–112). A large, single-center study re-
ported a 71% rate of freedom from recurrent VT
following multiple procedures during a mean follow-
up of nearly 5 years (112). There are very few reported
HCM and cardiac sarcoidosis patients treated with
catheter ablation; however, catheter ablation, often
substrate using a combined endocardial/epicardial approach,
JACC VOL. 70, NO. 23, 2017
DECEMBER 12, 2017:2924–41
appears to be reasonably efficacious and safe in
the treatment of drug-refractory VT in these patients
(32–36,41,42).
Although catheter ablation has not been proven to
improve mortality, there is evidence that a successful
ablation is associated with not only a higher rate of
freedom from VT, but also improved survival. A
retrospective analysis of outcomes of VT ablation
from high-volume centers demonstrated that freedom
from recurrent VT after catheter ablation is strongly
associated with a significant reduction in all-cause
mortality, independent of ejection fraction and heart
failure status (95). A meta-analysis of 8 cohort studies
with 928 post-infarction VT patients demonstrated
that complete noninducibility after ablation was
associated with a significant reduction in recurrent
ventricular arrhythmias when compared with partial
success (odds ratio [OR]: 0.49; 95% CI: 0.29 to 0.84;
p ¼ 0.009) or procedure failure (OR: 0.10; 95% CI: 0.06
to 0.18; p < 0.001) (113). Importantly, noninducibility
translated to a significant reduction in all-cause mor-
tality compared with either partial success (OR: 0.59;
95% CI: 0.36 to 0.98; p ¼ 0.04) or failed ablation
(OR: 0.32; 95% CI: 0.10 to 0.99; p ¼ 0.049). Similarly,
in a multicenter study of ischemic cardiomyopathy
patients, noninducibility was associated with a 35%
reduction in mortality (114). A similar finding has been
reported in dilated cardiomyopathy patients (103).
However, it should be recognized that all of the
studies indicating improved survival with successful
VT ablation (i.e., noninducibility) are nonrandomized.
It is also important to note that early referral of pa-
tients for catheter ablation is associated with
improved freedom from VT compared with later
referral when arrhythmic burden and substrate
severity are higher (115).
Major procedure-related complications may occur
in w7% of patients (9,62,95,116). Cardiac perforation
occurs in 1.5%, major vascular injury in 2.3%, and
death in up to 3%. Other complications include un-
controllable VT in up to 2.6%, stroke or transient
ischemic attack in 0.5%, heart block in 0.9%, and
coronary artery injury in 0.2%. Acute hemodynamic
decompensation, defined as persistent hypotension
despite vasopressors requiring mechanical support or
discontinuation of the procedure, is reported to occur
in 11% of patients and portends increased mortality
(81). Although these risks are not inconsequential, it
is important to remember that these patients have a
life-threatening condition that, if untreated, is likely
to culminate in mortality.
To identify patients at highest risk for hemodynamic
decompensation, the PAAINESD risk score (Pulmonary
disease, Age >60 years, general Anesthesia, Ischemic
Dukkipati et al. 2935
Catheter Ablation of VT in Structural Heart Disease
cardiomyopathy, New York Heart Association func-
tional class III or IV, Ejection fraction <25%, VT Storm,
Diabetes mellitus) has been developed (81). This risk
score may be useful to not only prospectively identify
high-risk patients likely to benefit from hemodynamic
support during ablation, but also identify patients that
should undergo multidisciplinary evaluation (i.e.,
heart failure and cardiothoracic surgery) for perma-
nent LVAD or heart transplantation in the case that
hemodynamic decompensation should occur during or
following VT ablation. The reported 1-year mortality
rate following VT ablation is 18%, with a primary
mechanism of death of either recurrent VT (37.5%) or
refractory heart failure (35%) (9). Early mortality
(#30 days) following VT ablation occurs in 5% of pa-
tients, with more than one-half of patients dying
before hospital discharge (116). The primary mecha-
nism of early mortality is also refractory VT or
advanced heart failure. Predictors of early mortality
include LVEF, chronic kidney disease, presentation
with VT storm, and presence of unmappable VTs (116).
The outcomes of patients with structural heart
disease undergoing ablation of PVCs resulting in LV
dysfunction and polymorphic VT/VF is more favor-
able (reviewed earlier in Part I).
ADJUNCTIVE THERAPIES AND
FUTURE DIRECTIONS
The efficacy of catheter ablation is occasionally
limited by the presence of intramyocardial VT circuits
unreachable with standard irrigated radiofrequency
ablation catheters. In these situations, ancillary
techniques have been used:
1. Transcoronary ethanol ablation requires identifi-
cation of a coronary arterial branch with a distri-
bution in the region of the VT circuit, and injection
of ethanol via an occlusive balloon catheter to
cause intramural myocardial necrosis. This tech-
nique, although useful for the eradication of
intramyocardial VT, is limited by dependence on a
coronary anatomy with the requisite distribution
(117) (Figure 6).
2. Bipolar radiofrequency ablation is performed be-
tween 2 ablation catheters positioned on opposing
ventricular walls adjacent to the intramyocardial
VT circuit. Bipolar ablation produces larger and
more transmural lesions compared with standard
(unipolar) ablation performed sequentially on
opposing sides of the target tissue and can be used
to terminate VT when standard methods fail (118)
(Figure 7).
3. Intramural needle ablation catheters are designed
to allow a needle electrode to be advanced into the
2936 Dukkipati et al. JACC VOL. 70, NO. 23, 2017

Catheter Ablation of VT in Structural Heart Disease DECEMBER 12, 2017:2924–41

F I G U R E 6 Transcoronary Ethanol Ablation for VT Related to Isolated Septal Scar in Nonischemic Cardiomyopathy

(A) A bipolar voltage map of the left ventricle (right anterior oblique view) demonstrates a large area of basal and septal scar (red area).
Despite multiple radiofrequency ablation lesions (red points) on the LV septum and RV septum (not shown), VT remained inducible. (B)
Transcoronary ethanol ablation was performed to target the inducible VT. An occlusive balloon was positioned in the first septal perforator of
the left anterior descending artery and ethanol was injected (arrow) into the artery to target the myocardium in the distribution of the VT
exit site (dashed circle). Abbreviations as in Figures 4 and 5.

ventricular wall to create large intramural radio-
frequency lesions (119,120). Although promising for
the treatment of intramural VT circuits, these
techniques create larger lesions and may increase
the risk of complications including cardiac perfo-
ration, atrioventricular block, and worsening LV
function. Although these techniques are useful for
the termination of any given VT, none has been
shown to improve long-term freedom from VT. As
sparse data exist, the efficacy and safety of bipolar
catheter ablation and intramural needle ablation
are being further evaluated in nonrandomized
single and multicenter studies (Bipolar Ventricular
Tachycardia [VT] Study, NCT02374476; Intramural
Needle Ablation for Ventricular Tachycardia,
NCT02799693; Intramural Needle Ablation for the
Treatment of Refractory Ventricular Arrhythmias,
NCT03204981).
Stereotactic radioablation is commonly used to
noninvasively treat solid tumors, and has recently
been considered for the treatment of ventricular
tachycardia (121,122). Multiple low-dose ionizing ra-
diation beams (photons from x-rays or gamma rays)
are delivered from multiple angles to focus concen-
trated ablative energy on target tissue while
minimizing damage to adjacent tissue. The target
arrhythmogenic substrate is identified using imaging
(i.e., CMR, computed tomography, and positron-
emission tomography). The mechanism of tissue
death is apoptosis and microvascular injury rather
than thermal as with radiofrequency ablation, and
typically has a delayed manifestation (days to
months). Clinical data is very limited, but ongoing
multicenter trials will provide more insight into the
safety and efficacy of this treatment modality.
Autonomic modulation targets the known central
role that the autonomic nervous system plays in the
initiation and maintenance of ventricular arrhythmias.
The most common neuromodulation method is left or
bilateral cardiac sympathetic denervation (CSD), which
involves the resection of the lower third of the stellate
ganglia, T2 to T4 thoracic ganglia, and the nerve of
Kuntz when present (123,124). In a recent retrospective
multicenter study of 121 patients with refractory VT or
VT storm, CSD was associated with a 1-year freedom
from sustained VT or ICD shocks of 58%, and freedom
from ICD shocks, sustained VT, death, or heart trans-
plantation of 50% (124). Bilateral CSD was superior to
left CSD. Another method of neuromodulation, renal
sympathetic denervation, is conceptually attractive,
but is only supported by sparse data.
JACC VOL. 70, NO. 23, 2017 Dukkipati et al. 2937
DECEMBER 12, 2017:2924–41 Catheter Ablation of VT in Structural Heart Disease

F I G U R E 7 Bipolar Radiofrequency Ablation for VT Related to Isolated Septal Scar in Nonischemic Cardiomyopathy

Bipolar voltage maps in (A) the right anterior oblique view and (B) the left anterior oblique view demonstrate a large area of septal scar
(red area). This patient required multiple bipolar radiofrequency ablation lesions (purple points) to render VT noninducible. Bipolar
radiofrequency ablation was performed between a catheter positioned on the RV septum (yellow arrow) and LV septum (white arrow).
The thickness of the myocardium at this site was 19.0 mm. Abbreviations as in Figures 4 and 5.

CONCLUSIONS presenting with VT storm, advanced heart failure with

Catheter ablation of ventricular tachycardia in pa-
tients with structural heart disease can significantly
reduce the incidence of recurrent ventricular ar-
rhythmias. It is best used as an adjunct to ICDs, and as
an alternative or adjunct to antiarrhythmic drugs.
Certain patients with left ventricular dysfunction due
to frequent ventricular ectopy benefit from catheter
ablation as a primary treatment strategy, because
ventricular dysfunction may be reversible, thereby
obviating the need for ICD therapy.
Although catheter ablation reduces recurrent ven-
tricular arrhythmias, randomized controlled trials
powered to examine mortality reduction have not been
performed. However, observational studies indicate
that successful catheter ablation reduces mortality.
Earlier referral for VT ablation is strongly associated
with improved outcomes when compared to later
referral, where arrhythmic burden and substrate
severity are higher. Overall, catheter ablation in this
population has an acceptable risk, but patients
severely reduced LV function, and certain other
comorbidities are at increased risk for procedure-
related hemodynamic decompensation; they may
benefit from percutaneous hemodynamic support
during the procedure. These patients should undergo
pre-procedure optimization of heart failure and a
multidisciplinary evaluation for advanced therapies
should hemodynamic decompensation occur. The
rates of ventricular arrhythmia recurrence are signifi-
cant, partially due to the inability to ablate VT circuits
that are present deep within the myocardium. In these
situations, adjunctive therapies such as cardiac sym-
pathetic denervation are potential options. Techno-
logical advancements in substrate imaging, mapping,
and ablation to improve outcomes are in development.
ADDRESS FOR CORRESPONDENCE: Dr. Vivek Y.
Reddy, Icahn School of Medicine at Mount Sinai
Medical Center, One Gustave L. Levy Place, Box 1030,
New York, New York 10029. E-mail: vivek.reddy@
mountsinai.org.

REFERENCES

1. de Bakker JM, van Capelle FJ, Janse MJ, et al.
Reentry as a cause of ventricular tachycardia in
patients with chronic ischemic heart disease:
electrophysiologic and anatomic correlation.
Circulation 1988;77:589–606.
2. Peters NS, Green CR, Poole-Wilson PA,
Severs NJ. Reduced content of connexin43 gap
junctions in ventricular myocardium from hyper-
trophied and ischemic human hearts. Circulation
1993;88:864–75.
3. de Bakker JM, van Capelle FJ, Janse MJ, et al.
Macroreentry in the infarcted human heart: the
mechanism of ventricular tachycardias with a
“focal” activation pattern. J Am Coll Cardiol 1991;
18:1005–14.
2938 Dukkipati et al.
Catheter Ablation of VT in Structural Heart Disease
4. de Bakker JM, van Capelle FJ, Janse MJ, et al.
Slow conduction in the infarcted human heart.
’Zigzag’ course of activation. Circulation 1993;88:
915–26.
5. Cao JM, Fishbein MC, Han JB, et al. Relationship
between regional cardiac hyperinnervation and
ventricular arrhythmia. Circulation 2000;101:
1960–9.
6. Ajijola OA, Yagishita D, Reddy NK, et al.
Remodeling of stellate ganglion neurons after
spatially targeted myocardial infarction: neuro-
peptide and morphologic changes. Heart Rhythm
2015;12:1027–35.
7. Rajendran PS, Nakamura K, Ajijola OA, et al.
Myocardial infarction induces structural and
functional remodelling of the intrinsic cardiac
nervous system. J Physiol 2016;594:321–41.
8. Ajijola OA, Lux RL, Khahera A, et al. Sympa-
thetic modulation of electrical activation in normal
and infarcted myocardium: implications for
arrhythmogenesis. Am J Physiol Heart Circ Physiol
2017;312:H608–21.
9. Stevenson WG, Wilber DJ, Natale A, et al. Irri-
gated radiofrequency catheter ablation guided by
electroanatomic mapping for recurrent ventricular
tachycardia after myocardial infarction: the
multicenter thermocool ventricular tachycardia
ablation trial. Circulation 2008;118:2773–82.
10. Anter E, Tschabrunn CM, Buxton AE,
Josephson ME. High-resolution mapping of post-
infarction reentrant ventricular tachycardia: elec-
trophysiological characterization of the circuit.
Circulation 2016;134:314–27.
11. Haissaguerre M, Shah DC, Jais P, et al. Role of
Purkinje conducting system in triggering of idio-
pathic ventricular fibrillation. Lancet 2002;359:
677–8.
12. Bansch D, Oyang F, Antz M, et al. Successful
catheter ablation of electrical storm after
myocardial infarction. Circulation 2003;108:
3011–6.
13. Marrouche NF, Verma A, Wazni O, et al. Mode
of initiation and ablation of ventricular fibrillation
storms in patients with ischemic cardiomyopathy.
J Am Coll Cardiol 2004;43:1715–20.
14. Szumowski L, Sanders P, Walczak F, et al.
Mapping and ablation of polymorphic ventricular
tachycardia after myocardial infarction. J Am Coll
Cardiol 2004;44:1700–6.
15. Lazzara R, el-Sherif N, Scherlag BJ. Electro-
physiological properties of canine Purkinje cells in
one-day-old myocardial infarction. Circ Res 1973;
33:722–34.
16. Xing D, Martins JB. Triggered activity due to
delayed afterdepolarizations in sites of focal origin
of ischemic ventricular tachycardia. Am J Physiol
Heart Circ Physiol 2004;287:H2078–84.
17. Bogun F, Good E, Reich S, et al. Role of Pur-
kinje fibers in post-infarction ventricular tachy-
cardia. J Am Coll Cardiol 2006;48:2500–7.
18. Nakayama Y, Shimizu G, Hirota Y, et al. Func-
tional and histopathologic correlation in patients
with dilated cardiomyopathy: an integrated eval-
uation by multivariate analysis. J Am Coll Cardiol
1987;10:186–92.
19. Assomull RG, Prasad SK, Lyne J, et al. Car-
diovascular magnetic resonance, fibrosis, and
prognosis in dilated cardiomyopathy. J Am Coll
Cardiol 2006;48:1977–85.
20. McCrohon JA, Moon JC, Prasad SK, et al. Dif-
ferentiation of heart failure related to dilated
cardiomyopathy and coronary artery disease using
gadolinium-enhanced cardiovascular magnetic
resonance. Circulation 2003;108:54–9.
21. Delacretaz E, Stevenson WG, Ellison KE,
Maisel WH, Friedman PL. Mapping and radio-
frequency catheter ablation of the three types of
sustained monomorphic ventricular tachycardia in
nonischemic heart disease. J Cardiovasc Electro-
physiol 2000;11:11–7.
22. Oloriz T, Silberbauer J, Maccabelli G, et al.
Catheter ablation of ventricular arrhythmia in
nonischemic cardiomyopathy: anteroseptal versus
inferolateral scar sub-types. Circ Arrhythm Elec-
trophysiol 2014;7:414–23.
23. Soejima K, Stevenson WG, Sapp JL, Selwyn AP,
Couper G, Epstein LM. Endocardial and epicardial
radiofrequency ablation of ventricular tachycardia
associated with dilated cardiomyopathy: the
importance of low-voltage scars. J Am Coll Cardiol
2004;43:1834–42.
24. Hsia HH, Callans DJ, Marchlinski FE. Charac-
terization of endocardial electrophysiological
substrate in patients with nonischemic cardiomy-
opathy and monomorphic ventricular tachycardia.
Circulation 2003;108:704–10.
25. Bogun FM, Desjardins B, Good E, et al.
Delayed-enhanced magnetic resonance imaging in
nonischemic cardiomyopathy: utility for identi-
fying the ventricular arrhythmia substrate. J Am
Coll Cardiol 2009;53:1138–45.
26. Marcus FI, McKenna WJ, Sherrill D, et al.
Diagnosis of arrhythmogenic right ventricular
cardiomyopathy/dysplasia: proposed modification
of the task force criteria. Circulation 2010;121:
1533–41.
27. Marchlinski FE, Zado E, Dixit S, et al. Electro-
anatomic substrate and outcome of catheter
ablative therapy for ventricular tachycardia in
setting of right ventricular cardiomyopathy. Cir-
culation 2004;110:2293–8.
28. Te Riele AS, James CA, Philips B, et al.
Mutation-positive arrhythmogenic right ventricu-
lar dysplasia/cardiomyopathy: the triangle of
dysplasia displaced. J Cardiovasc Electrophysiol
2013;24:1311–20.
29. Link MS, Laidlaw D, Polonsky B, et al. Ven-
tricular arrhythmias in the North American
multidisciplinary study of ARVC: predictors,
characteristics, and treatment. J Am Coll Car-
diol 2014;64:119–25.
30. Maron BJ, Spirito P, Shen WK, et al. Implant-
able cardioverter-defibrillators and prevention of
sudden cardiac death in hypertrophic cardiomy-
opathy. JAMA 2007;298:405–12.
31. Link MS, Bockstall K, Weinstock J, et al. Ven-
tricular tachyarrhythmias in patients with hyper-
trophic cardiomyopathy and defibrillators: triggers,
treatment and implications. J Cardiovasc Electro-
physiol 2017;28:531–7.
JACC VOL. 70, NO. 23, 2017
DECEMBER 12, 2017:2924–41
32. Rowin EJ, Maron BJ, Haas TS, et al. Hyper-
trophic cardiomyopathy with left ventricular apical
aneurysm: implications for risk stratification and
management. J Am Coll Cardiol 2017;69:761–73.
33. Furushima H, Chinushi M, Iijima K, et al. Ven-
tricular tachyarrhythmia associated with hyper-
trophic cardiomyopathy: incidence, prognosis, and
relation to type of hypertrophy. J Cardiovasc
Electrophysiol 2010;21:991–9.
34. Dukkipati SR, d’Avila A, Soejima K, et al. Long-
term outcomes of combined epicardial and endo-
cardial ablation of monomorphic ventricular
tachycardia related to hypertrophic cardiomyopa-
thy. Circ Arrhythm Electrophysiol 2011;4:185–94.
35. Santangeli P, Di Biase L, Lakkireddy D, et al.
Radiofrequency catheter ablation of ventricular
arrhythmias in patients with hypertrophic cardio-
myopathy: safety and feasibility. Heart Rhythm
2010;7:1036–42.
36. Inada K, Seiler J, Roberts-Thomson KC, et al.
Substrate characterization and catheter ablation
for monomorphic ventricular tachycardia in pa-
tients with apical hypertrophic cardiomyopathy.
J Cardiovasc Electrophysiol 2011;22:41–8.
37. Iwai K, Takemura T, Kitaichi M, Kawabata Y,
Matsui Y. Pathological studies on sarcoidosis au-
topsy. II. Early change, mode of progression and
death pattern. Acta Pathol Jpn 1993;43:377–85.
38. Birnie DH, Sauer WH, Bogun F, et al. HRS
expert consensus statement on the diagnosis and
management of arrhythmias associated with car-
diac sarcoidosis. Heart Rhythm 2014;11:1305–23.
39. Doughan AR, Williams BR. Cardiac sarcoidosis.
Heart 2006;92:282–8.
40. Furushima H, Chinushi M, Sugiura H, Kasai H,
Washizuka T, Aizawa Y. Ventricular tachyar-
rhythmia associated with cardiac sarcoidosis: its
mechanisms and outcome. Clin Cardiol 2004;27:
217–22.
41. Muser D, Santangeli P, Pathak RK, et al. Long-
term outcomes of catheter ablation of ventricular
tachycardia in patients with cardiac sarcoidosis.
Circ Arrhythm Electrophysiol 2016;9:e004333.
42. Kumar S, Barbhaiya C, Nagashima K, et al.
Ventricular tachycardia in cardiac sarcoidosis:
characterization of ventricular substrate and out-
comes of catheter ablation. Circ Arrhythm Elec-
trophysiol 2015;8:87–93.
43. Nunes MC, Dones W, Morillo CA, Encina JJ,
Ribeiro AL. Chagas disease: an overview of clinical
and epidemiological aspects. J Am Coll Cardiol
2013;62:767–76.
44. Prata A. Clinical and epidemiological aspects
of Chagas disease. Lancet Infect Dis 2001;1:
92–100.
45. Sarabanda AV, Sosa E, Simoes MV,
Figueiredo GL, Pintya AO, Marin-Neto JA. Ven-
tricular tachycardia in Chagas’ disease: a compar-
ison of clinical, angiographic, electrophysiologic
and myocardial perfusion disturbances between
patients presenting with either sustained or non-
sustained forms. Int J Cardiol 2005;102:9–19.
46. Scanavacca M, Sosa E. Epicardial ablation of
ventricular tachycardia in Chagas heart disease.
Card Electrophysiol Clin 2010;2:55–67.
JACC VOL. 70, NO. 23, 2017
DECEMBER 12, 2017:2924–41
47. Sosa E, Scanavacca M, d’Avila A, Pilleggi F.
A new technique to perform epicardial mapping in
the electrophysiology laboratory. J Cardiovasc
Electrophysiol 1996;7:531–6.
48. Sosa E, Scanavacca M, D’Avila A, et al. Endo-
cardial and epicardial ablation guided by nonsur-
gical transthoracic epicardial mapping to treat
recurrent ventricular tachycardia. J Cardiovasc
Electrophysiol 1998;9:229–39.
49. Epstein AE, DiMarco JP, Ellenbogen KA, et al.
ACC/AHA/HRS 2008 guidelines for device-based
therapy of cardiac rhythm abnormalities: a report
of the American College of Cardiology/American
Heart Association Task Force on Practice Guide-
lines (Writing Committee to Revise the ACC/AHA/
NASPE 2002 Guideline Update for Implantation
of Cardiac Pacemakers and Antiarrhythmia De-
vices) developed in collaboration with the
American Association for Thoracic Surgery and
Society of Thoracic Surgeons. J Am Coll Cardiol
2008;51:e1–62.
50. Epstein AE, DiMarco JP, Ellenbogen KA, et al.
2012 ACCF/AHA/HRS focused update incorporated
into the ACCF/AHA/HRS 2008 guidelines for
device-based therapy of cardiac rhythm abnor-
malities: a report of the American College of Car-
diology Foundation/American Heart Association
Task Force on Practice Guidelines and the Heart
Rhythm Society. J Am Coll Cardiol 2013;61:e6–75.
51. Kusumoto FM, Calkins H, Boehmer J, et al.
HRS/ACC/AHA expert consensus statement on the
use of implantable cardioverter-defibrillator ther-
apy in patients who are not included or not well
represented in clinical trials. J Am Coll Cardiol
2014;64:1143–77.
52. Bardy GH, Lee KL, Mark DB, et al. Amiodarone
or an implantable cardioverter-defibrillator for
congestive heart failure. N Engl J Med 2005;352:
225–37.
53. Bristow MR, Saxon LA, Boehmer J, et al. Car-
diac-resynchronization therapy with or without an
implantable defibrillator in advanced chronic heart
failure. N Engl J Med 2004;350:2140–50.
54. Kadish A, Dyer A, Daubert JP, et al. Prophy-
lactic defibrillator implantation in patients with
nonischemic dilated cardiomyopathy. N Engl J
Med 2004;350:2151–8.
55. Kober L, Thune JJ, Nielsen JC, et al. Defibril-
lator Implantation in Patients with Nonischemic
Systolic Heart Failure. N Engl J Med 2016;375:
1221–30.
56. Golwala H, Bajaj NS, Arora G, Arora P.
Implantable cardioverter-defibrillator for non-
ischemic cardiomyopathy: an updated meta-anal-
ysis. Circulation 2017;135:201–3.
57. Moss AJ, Schuger C, Beck CA, et al. Reduction
in inappropriate therapy and mortality through
ICD programming. N Engl J Med 2012;367:
2275–83.
58. Gasparini M, Proclemer A, Klersy C, et al.
Effect of long-detection interval vs standard-
detection interval for implantable cardioverter-
defibrillators on antitachycardia pacing and shock
delivery: the ADVANCE III randomized clinical trial.
JAMA 2013;309:1903–11.
59. Fonarow GC, Yancy CW, Hernandez AF,
Peterson ED, Spertus JA, Heidenreich PA.
Potential impact of optimal implementation of
evidence-based heart failure therapies on mortal-
ity. Am Heart J 2011;161:1024–30.
60. Connolly SJ, Dorian P, Roberts RS, et al.
Comparison of beta-blockers, amiodarone plus
beta-blockers, or sotalol for prevention of shocks
from implantable cardioverter defibrillators: the
OPTIC Study: a randomized trial. JAMA 2006;295:
165–71.
61. Santangeli P, Muser D, Maeda S, et al.
Comparative effectiveness of antiarrhythmic drugs
and catheter ablation for the prevention of
recurrent ventricular tachycardia in patients with
implantable cardioverter-defibrillators: a system-
atic review and meta-analysis of randomized
controlled trials. Heart Rhythm 2016;13:1552–9.
62. Sapp JL, Wells GA, Parkash R, et al. Ventricular
tachycardia ablation versus escalation of antiar-
rhythmic drugs. N Engl J Med 2016;375:111–21.
63. Reddy VY, Reynolds MR, Neuzil P, et al. Pro-
phylactic catheter ablation for the prevention of
defibrillator therapy. N Engl J Med 2007;357:
2657–65.
64. Kuck KH, Schaumann A, Eckardt L, et al.
Catheter ablation of stable ventricular tachycardia
before defibrillator implantation in patients with
coronary heart disease (VTACH): a multicentre
randomised controlled trial. Lancet 2010;375:
31–40.
65. Kuck KH, Tilz RR, Deneke T, et al. Impact of
substrate modification by catheter ablation on
implantable cardioverter-defibrillator in-
terventions in patients with unstable ventricular
arrhythmias and coronary artery disease: results
from the multicenter randomized controlled SMS
(Substrate Modification Study). Circ Arrhythm
Electrophysiol 2017;10:e004422.
66. Aliot EM, Stevenson WG, Almendral-
Garrote JM, et al. EHRA/HRS expert consensus on
catheter ablation of ventricular arrhythmias:
developed in a partnership with the European
Heart Rhythm Association (EHRA), a Registered
Branch of the European Society of Cardiology
(ESC), and the Heart Rhythm Society (HRS); in
collaboration with the American College of Car-
diology (ACC) and the American Heart Association
(AHA). Europace 2009;11:771–817.
67. Pedersen CT, Kay GN, Kalman J, et al. EHRA/
HRS/APHRS expert consensus on ventricular ar-
rhythmias. Heart Rhythm 2014;11:e166–96.
68. Priori SG, Blomstrom-Lundqvist C, Mazzanti A,
et al. 2015 ESC guidelines for the management of
patients with ventricular arrhythmias and the
prevention of sudden cardiac death: the Task
Force for the Management of Patients with Ven-
tricular Arrhythmias and the Prevention of Sudden
Cardiac Death of the European Society of Cardi-
ology (ESC). Eur Heart J 2015;36:2793–867.
69. Marchlinski FE, Callans DJ, Gottlieb CD,
Zado E. Linear ablation lesions for control of
unmappable ventricular tachycardia in patients
with ischemic and nonischemic cardiomyopathy.
Circulation 2000;101:1288–96.
70. Cassidy DM, Vassallo JA, Buxton AE,
Doherty JU, Marchlinski FE, Josephson ME. The
value of catheter mapping during sinus rhythm to
Dukkipati et al. 2939
Catheter Ablation of VT in Structural Heart Disease
localize site of origin of ventricular tachycardia.
Circulation 1984;69:1103–10.
71. Cassidy DM, Vassallo JA, Miller JM, et al.
Endocardial catheter mapping in patients in sinus
rhythm: relationship to underlying heart disease
and ventricular arrhythmias. Circulation 1986;73:
645–52.
72. Bogun F, Good E, Reich S, et al. Isolated po-
tentials during sinus rhythm and pace-mapping
within scars as guides for ablation of post-
infarction ventricular tachycardia. J Am Coll Car-
diol 2006;47:2013–9.
73. Hsia HH, Lin D, Sauer WH, Callans DJ,
Marchlinski FE. Relationship of late potentials to
the ventricular tachycardia circuit defined by
entrainment. J Interv Card Electrophysiol 2009;
26:21–9.
74. Jais P, Maury P, Khairy P, et al. Elimination of
local abnormal ventricular activities: a new end
point for substrate modification in patients with
scar-related ventricular tachycardia. Circulation
2012;125:2184–96.
75. Irie T, Yu R, Bradfield JS, et al. Relationship
between sinus rhythm late activation zones and
critical sites for scar-related ventricular tachy-
cardia: systemic analysis of isochronal late acti-
vation mapping. Circ Arrhythm Electrophysiol
2015;8:390–9.
76. Stevenson WG, Friedman PL, Sager PT, et al.
Exploring postinfarction reentrant ventricular
tachycardia with entrainment mapping. J Am Coll
Cardiol 1997;29:1180–9.
77. Brunckhorst CB, Stevenson WG, Soejima K,
et al. Relationship of slow conduction detected by
pace-mapping to ventricular tachycardia re-entry
circuit sites after infarction. J Am Coll Cardiol
2003;41:802–9.
78. Brunckhorst CB, Delacretaz E, Soejima K,
Maisel WH, Friedman PL, Stevenson WG. Identifi-
cation of the ventricular tachycardia isthmus after
infarction by pace mapping. Circulation 2004;110:
652–9.
79. Miller MA, Dukkipati SR, Mittnacht AJ, et al.
Activation and entrainment mapping of hemody-
namically unstable ventricular tachycardia using a
percutaneous left ventricular assist device. J Am
Coll Cardiol 2011;58:1363–71.
80. Miller MA, Dukkipati SR, Chinitz JS, et al.
Percutaneous hemodynamic support with Impella
2.5 during scar-related ventricular tachycardia
ablation (PERMIT 1). Circ Arrhythm Electrophysiol
2013;6:151–9.
81. Santangeli P, Muser D, Zado ES, et al. Acute
hemodynamic decompensation during catheter
ablation of scar-related ventricular tachycardia:
incidence, predictors, and impact on mortality.
Circ Arrhythm Electrophysiol 2015;8:68–75.
82. Kusa S, Miller MA, Whang W, et al. Outcomes
of ventricular tachycardia ablation using percuta-
neous left ventricular assist devices. Circ Arrhythm
Electrophysiol 2017;10:e004717.
83. Baratto F, Pappalardo F, Oloriz T, et al.
Extracorporeal membrane oxygenation for he-
modynamic support of ventricular tachycardia
ablation. Circ Arrhythm Electrophysiol 2016;9:
e004492.
2940 Dukkipati et al.
Catheter Ablation of VT in Structural Heart Disease
84. Balasundaram R, Rao HB, Kalavakolanu S,
Narasimhan C. Catheter ablation of bundle branch
reentrant ventricular tachycardia. Heart Rhythm
2008;5:S68–72.
85. Di Biase L, Santangeli P, Burkhardt DJ, et al.
Endo-epicardial homogenization of the scar
versus limited substrate ablation for the treat-
ment of electrical storms in patients with
ischemic cardiomyopathy. J Am Coll Cardiol
2012;60:132–41.
86. Soejima K, Couper G, Cooper JM, Sapp JL,
Epstein LM, Stevenson WG. Subxiphoid surgical
approach for epicardial catheter-based mapping
and ablation in patients with prior cardiac surgery
or difficult pericardial access. Circulation 2004;
110:1197–201.
87. Michowitz Y, Mathuria N, Tung R, et al. Hybrid
procedures for epicardial catheter ablation of
ventricular tachycardia: value of surgical access.
Heart Rhythm 2010;7:1635–43.
88. Siontis KC, Kim HM, Sharaf Dabbagh G, et al.
Association of preprocedural cardiac magnetic
resonance imaging with outcomes of ventricular
tachycardia ablation in patients with idiopathic
dilated cardiomyopathy. Heart Rhythm 2017;14:
1487–93.
89. Berruezo A, Mont L, Nava S, Chueca E,
Bartholomay E, Brugada J. Electrocardiographic
recognition of the epicardial origin of ventricular
tachycardias. Circulation 2004;109:1842–7.
90. Daniels DV, Lu YY, Morton JB, et al. Idiopathic
epicardial left ventricular tachycardia originating
remote from the sinus of Valsalva: electrophysio-
logical characteristics, catheter ablation, and
identification from the 12-lead electrocardiogram.
Circulation 2006;113:1659–66.
91. Valles E, Bazan V, Marchlinski FE. ECG criteria
to identify epicardial ventricular tachycardia in
nonischemic cardiomyopathy. Circ Arrhythm
Electrophysiol 2010;3:63–71.
92. Martinek M, Stevenson WG, Inada K,
Tokuda M, Tedrow UB. QRS characteristics fail to
reliably identify ventricular tachycardias that
require epicardial ablation in ischemic heart dis-
ease. J Cardiovasc Electrophysiol 2012;23:
188–93.
93. Piers SR, Silva Mde R, Kapel GF, Trines SA,
Schalij MJ, Zeppenfeld K. Endocardial or
epicardial ventricular tachycardia in non-
ischemic cardiomyopathy? The role of 12-lead
ECG criteria in clinical practice. Heart Rhythm
2014;11:1031–9.
94. Tanner H, Hindricks G, Volkmer M, et al.
Catheter ablation of recurrent scar-related ven-
tricular tachycardia using electroanatomical map-
ping and irrigated ablation technology: results of
the prospective multicenter Euro-VT-study.
J Cardiovasc Electrophysiol 2010;21:47–53.
95. Tung R, Vaseghi M, Frankel DS, et al.
Freedom from recurrent ventricular tachycardia
after catheter ablation is associated with
improved survival in patients with structural
heart disease: An International VT Ablation
Center Collaborative Group study. Heart Rhythm
2015;12:1997–2007.
96. Marchlinski FE, Haffajee CI, Beshai JF, et al.
Long-term success of irrigated radiofrequency
catheter ablation of sustained ventricular tachy-
cardia: post-approval THERMOCOOL VT Trial.
J Am Coll Cardiol 2016;67:674–83.
97. Berruezo A, Fernandez-Armenta J, Andreu D,
et al. Scar dechanneling: new method for scar-
related left ventricular tachycardia substrate
ablation. Circ Arrhythm Electrophysiol 2015;8:
326–36.
98. Silberbauer J, Oloriz T, Maccabelli G, et al.
Noninducibility and late potential abolition: a
novel combined prognostic procedural end point
for catheter ablation of postinfarction ventricular
tachycardia. Circ Arrhythm Electrophysiol 2014;7:
424–35.
99. Komatsu Y, Maury P, Sacher F, et al. Impact of
substrate-based ablation of ventricular tachycardia
on cardiac mortality in patients with implantable
cardioverter-defibrillators. J Cardiovasc Electro-
physiol 2015;26:1230–8.
100. Di Biase L, Burkhardt JD, Lakkireddy D, et al.
Ablation of stable VTs versus substrate ablation in
ischemic cardiomyopathy: The VISTA Randomized
Multicenter Trial. J Am Coll Cardiol 2015;66:
2872–82.
101. Muser D, Santangeli P, Castro SA, et al. Long-
term outcome after catheter ablation of ventric-
ular tachycardia in patients with nonischemic
dilated cardiomyopathy. Circ Arrhythm Electro-
physiol 2016;9:e004328.
102. Haqqani HM, Tschabrunn CM, Tzou WS, et al.
Isolated septal substrate for ventricular tachy-
cardia in nonischemic dilated cardiomyopathy:
incidence, characterization, and implications.
Heart Rhythm 2011;8:1169–76.
103. Dinov B, Arya A, Schratter A, et al. Catheter
ablation of ventricular tachycardia and mortality in
patients with nonischemic dilated cardiomyopa-
thy: can noninducibility after ablation be a pre-
dictor for reduced mortality? Circ Arrhythm
Electrophysiol 2015;8:598–605.
104. Dinov B, Fiedler L, Schonbauer R, et al.
Outcomes in catheter ablation of ventricular
tachycardia in dilated nonischemic cardiomyopa-
thy compared with ischemic cardiomyopathy: re-
sults from the Prospective Heart Centre of Leipzig
VT (HELP-VT) Study. Circulation 2014;129:728–36.
105. Gokoglan Y, Mohanty S, Gianni C, et al. Scar
homogenization versus limited-substrate ablation
in patients with nonischemic cardiomyopathy and
ventricular tachycardia. J Am Coll Cardiol 2016;
68:1990–8.
106. Nakahara S, Tung R, Ramirez RJ, et al.
Characterization of the arrhythmogenic substrate
in ischemic and nonischemic cardiomyopathy im-
plications for catheter ablation of hemodynami-
cally unstable ventricular tachycardia. J Am Coll
Cardiol 2010;55:2355–65.
107. Dalal D, Jain R, Tandri H, et al. Long-term
efficacy of catheter ablation of ventricular tachy-
cardia in patients with arrhythmogenic right ven-
tricular dysplasia/cardiomyopathy. J Am Coll
Cardiol 2007;50:432–40.
108. Bai R, Di Biase L, Shivkumar K, et al. Ablation
of ventricular arrhythmias in arrhythmogenic right
ventricular dysplasia/cardiomyopathy: arrhythmia-
free survival after endo-epicardial substrate based
JACC VOL. 70, NO. 23, 2017
DECEMBER 12, 2017:2924–41
mapping and ablation. Circ Arrhythm Electrophysiol
2011;4:478–85.
109. Verma A, Kilicaslan F, Schweikert RA, et al.
Short- and long-term success of substrate-based
mapping and ablation of ventricular tachycardia
in arrhythmogenic right ventricular dysplasia. Cir-
culation 2005;111:3209–16.
110. Garcia FC, Bazan V, Zado ES, Ren JF,
Marchlinski FE. Epicardial substrate and outcome
with epicardial ablation of ventricular tachy-
cardia in arrhythmogenic right ventricular car-
diomyopathy/dysplasia. Circulation 2009;120:
366–75.
111. Philips B, Madhavan S, James C, et al. Out-
comes of catheter ablation of ventricular tachy-
cardia in arrhythmogenic right ventricular
dysplasia/cardiomyopathy. Circ Arrhythm Electro-
physiol 2012;5:499–505.
112. Santangeli P, Zado ES, Supple GE, et al. Long-
term outcome with catheter ablation of ventricu-
lar tachycardia in patients with arrhythmogenic
right ventricular cardiomyopathy. Circ Arrhythm
Electrophysiol 2015;8:1413–21.
113. Ghanbari H, Baser K, Yokokawa M, et al.
Noninducibility in postinfarction ventricular
tachycardia as an end point for ventricular tachy-
cardia ablation and its effects on outcomes: a
meta-analysis. Circ Arrhythm Electrophysiol 2014;
7:677–83.
114. Yokokawa M, Kim HM, Baser K, et al. Predic-
tive value of programmed ventricular stimulation
after catheter ablation of post-infarction ventric-
ular tachycardia. J Am Coll Cardiol 2015;65:
1954–9.
115. Frankel DS, Mountantonakis SE, Robinson MR,
Zado ES, Callans DJ, Marchlinski FE. Ventricular
tachycardia ablation remains treatment of last
resort in structural heart disease: earlier inter-
vention. J Cardiovasc Electrophysiol 2011;22:
1123–8.
116. Santangeli P, Frankel DS, Tung R, et al.
Early mortality after catheter ablation of ven-
tricular tachycardia in patients with structural
heart disease. J Am Coll Cardiol 2017;69:
2105–15.
117. Tokuda M, Sobieszczyk P, Eisenhauer AC,
et al. Transcoronary ethanol ablation for recurrent
ventricular tachycardia after failed catheter abla-
tion: an update. Circ Arrhythm Electrophysiol
2011;4:889–96.
118. Koruth JS, Dukkipati S, Miller MA, Neuzil P,
d’Avila A, Reddy VY. Bipolar irrigated radio-
frequency ablation: a therapeutic option for re-
fractory intramural atrial and ventricular tachycardia
circuits. Heart Rhythm 2012;9:1932–41.
119. Sapp JL, Beeckler C, Pike R, et al. Initial hu-
man feasibility of infusion needle catheter ablation
for refractory ventricular tachycardia. Circulation
2013;128:2289–95.
120. John RM, Connell J, Termin P, et al. Charac-
terization of warm saline-enhanced radiofrequency
ablation lesions in the infarcted porcine ventricular
myocardium. J Cardiovasc Electrophysiol 2014;25:
309–16.
121. Loo BW Jr., Soltys SG, Wang L, et al.
Stereotactic ablative radiotherapy for the
JACC VOL. 70, NO. 23, 2017
DECEMBER 12, 2017:2924–41
treatment of refractory cardiac ventricular
arrhythmia. Circ Arrhythm Electrophysiol 2015;
8:748–50.
122. Zei PC, Soltys S. Ablative radiotherapy as
a noninvasive alternative to catheter ablation
for cardiac arrhythmias. Curr Cardiol Rep
2017;19:79.
123. Vaseghi M, Gima J, Kanaan C, et al. Cardiac
sympathetic denervation in patients with re-
fractory ventricular arrhythmias or electrical
storm: intermediate and long-term follow-up.
Heart Rhythm 2014;11:360–6.
124. Vaseghi M, Barwad P, Malavassi Corrales FJ,
et al. Cardiac sympathetic denervation for
Dukkipati et al. 2941
Catheter Ablation of VT in Structural Heart Disease
refractory ventricular arrhythmias. J Am Coll Car-
diol 2017;69:3070–80.
KEY WORDS catheter ablation, PVCs,
structural heart disease, ventricular
fibrillation, ventricular tachycardia