Catheter Ablation of Ventricular Tachycardia in Structural ... · electrical conduction through the border zone pre-disposes to re-entrant VT (1–4). Additionally, there are adaptive

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STATE-OF-THE-ART REVIEW

Catheter Ablation of VentricularTachycardia in Structural Heart DiseaseIndications, 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

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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 anelevated risk for suddencardiacdeath (SCD), and implantable cardioverter-defibrillators

(ICDs) are themainstay of therapy. In these individuals, catheter ablationmaybeused 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 forsudden cardiac death (SCD) has led to an

increase in the use of implantable cardioverter-defibrillators (ICDs). Consequently, more individualssurvive ventricular tachycardia (VT) or ventricularfibrillation (VF) episodes. This, together with anincreased understanding of the mechanisms and sub-strates responsible for ventricular arrhythmias, hasled to a growth in catheter ablation as a treatmentmodality for VT. Catheter ablation is being increas-ingly performed as adjunctive therapy to prevent orreduce ICD therapies when antiarrhythmic drugs areineffective or not desired. However, there is oftenconfusion among practicing physicians regarding in-dications, outcomes, and patient populations thatare most likely to benefit. In this paper, we reviewthe mechanisms and substrates for ventricular

m the Helmsley Electrophysiology Center, Department of Cardiology, Icah

rk. Dr. Dukkipati has received a research grant from Biosense Webster.

bster and Abbott. Dr. Reddy has received research grants from and se

entific, and Abbott. All other authors have reported that they have no re

close. Roderick Tung, MD, served as Guest Editor for this paper.

nuscript received September 25, 2017; revised manuscript received Octob

arrhythmias that occur in the setting of structuralheart disease and discuss the role of catheter ablationand patient populations who are most likely tobenefit from this treatment modality.

MECHANISM AND SUBSTRATE FOR VT IN

STRUCTURAL HEART DISEASE

POST-MYOCARDIAL INFARCTION. The prototypical,and best understood, substrate for scar-related re-entrant VT is post-myocardial infarction (MI) VT.Following MI, ventricular myocardium can broadly beclassified as normal, dense scar, or border zonetissue—the latter consisting of interconnected sur-viving myocardial fibrils interspersed among a bed ofelectrically inert fibrotic tissue. Together withdecreased cell-to-cell coupling, partly related toaltered connexin 43 expression, slow and circuitous

n School of Medicine at Mount Sinai, New York, New

Dr. Koruth has served as a consultant for Biosense

rved as a consultant for Biosense Webster, Boston

lationships relevant to the contents of this paper to

er 11, 2017, accepted October 17, 2017.

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AB BR E V I A T I O N S

AND ACRONYM S

ARVC/D = arrhythmogenic

right ventricular

cardiomyopathy/dysplasia

CSD = cardiac sympathetic

denervation

DAD = delayed after

depolarizations

DCM = dilated cardiomyopathy

HCM = hypertrophic

cardiomyopathy

ICD = implantable

cardioverter-defibrillator

LAVA = local abnormal

ventricular activity

LVAD = left ventricular assist

device

MI = myocardial infarction

PVC = premature ventricular

contraction

SCD = sudden cardiac death

VF = ventricular fibrillation

ventricular tachycardia

J A C C V O L . 7 0 , N O . 2 3 , 2 0 1 7 Dukkipati et al.D E C E M B E R 1 2 , 2 0 1 7 : 2 9 2 4 – 4 1 Catheter Ablation of VT in Structural Heart Disease

2925

electrical conduction through the border zone pre-disposes to re-entrant VT (1–4). Additionally, thereare adaptive and maladaptive changes in cardiacautonomic innervation that also predispose to VT (5–8). Sympathetic and parasympathetic efferent inputsto the convergent local circuit neurons are increased,whereas afferent inputs from infarcted tissue aredecreased relative to those from the border zone andnormal tissue; this results in a heterogeneity ofautonomic innervation, contributing to the arrhyth-mogenic substrate (7).

Asmultiple pathways often exist, numerous circuitsare commonly present and manifest as multipleinducible VTs during electrophysiological testing (9).The 12-lead electrocardiogram (ECG) morphology ofeach VT depends on the exit of the re-entrant circuitinto the normal myocardium. Although most VT exitsites are subendocardial, midmyocardial or epicardialexit sites also exist. Surviving tissue in the border zonecan be identified based on its abnormal conductionproperties and characteristic electrograms (i.e., lateand fractionated potentials) (Figure 1) and is often thetarget for ablation.

Although this fundamental understanding of thepathophysiology of post-MI VT has not changed sincethe mid-1990s, recent post-MI mapping studies usingultra high-resolution mapping technologies havesuggested that patients may have few arrhythmogenicborder zone areas of relatively constrained size (10).These small, anatomically fixed areas display direc-tion- and rate-dependent slowing of conductionvelocity related to highly curved activation patterns inareas of voltage <0.1 mV, and ablation of these rela-tively small areas resulted in VT termination andnoninducibility. However, the generalizability of thisobservation is unknown and requires additional study.

In addition to scar-related re-entry, certain post-MIpatients may present with ventricular arrhythmiasrelated to the Purkinje system. First described in pa-tients with idiopathic polymorphic VT or VF, focalpremature ventricular contractions (PVCs) originatingfrom Purkinje fibers may serve as triggers for thesearrhythmias (11). Similarly, following MI, triggeredactivity (due to delayed after depolarizations) fromsurviving Purkinje fibers situated along the scarborder may cause focal PVCs that trigger polymorphicVT/VF (12–15). Additionally, focal VT originating fromthe Purkinje system in the setting of acute ischemiahas been attributed to triggered activity and delayedafter depolarizations (16), in contrast to a re-entrantmechanism that is responsible for monomorphic VTfollowing remote MI (17). Catheter ablation is possiblefor the treatment of these various Purkinje-relatedventricular arrhythmias.

Although best described following MI, anydisease process that predisposes to myocar-dial scar may cause re-entrant VT. Theseinclude dilated cardiomyopathy, arrhythmo-genic right ventricular cardiomyopathy/dysplasia (ARVC/D), hypertrophic cardiomy-opathy, cardiac sarcoidosis, Chagas disease,and surgically repaired congenital heart dis-ease. However, unlike post-MI scar, which hasa predilection for the subendocardium, scar inthese disease states may occur in mid-myocardial and epicardial locations. Indeed,epicardial catheter ablation is often requiredin these disease states. Although there is anassumption that all scar-related re-entry issimilar, there is a paucity of studies that reportdetailed activation mapping of the re-entrantcircuit across nonischemic substrates.

DILATED CARDIOMYOPATHY. The ventricularmyocardium of individuals with dilated car-diomyopathy (DCM) is histologically charac-terized by multiple regions of patchyinterstitial and replacement fibrosis, myofiber
disarray, and variable degrees of myocyte hypertrophyand atrophy (18). Cardiovascular myocardial reso-nance (CMR) with late gadolinium enhancementidentifies fibrosis in up to 41% and is an importantpredictor of sudden cardiac death and VT (19,20). Inearly studies, the mechanism of DCM-related VT wasestimated to be scar-related re-entry in 62%, focalautomaticity 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 theexclusion of most patients with hemodynamicallyunstable VT; more recent studies suggest that re-entryis by far the primary VTmechanism in DCM-VT. Unlikepost-MI scar that has a predilection for the sub-endocardium, scar in DCM may be midmyocardial orepicardial 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 ina subepicardial location and progresses towardthe endocardial surface. Although predominantlyinvolving the RV, left dominant and biventricularvariants also exist (26). Thus, the triangle ofdysplasia, which is classically described as involvingthe RV inflow tract, RV outflow tract, and RV apex, isnow thought to include the basal inferior RV, basalanterior RV, and posterolateral LV; the RV apex isspared until advanced stages of the disease (27,28).

VT =

FIGURE 1 Myocardial Scar and Substrate for Re-Entrant VT

V1

MAP

V1

MAP

V1

*

*

MAP

Fractionated Potential

Late Potential

LAVA

NormalMyocardium

Border Zone

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.

Dukkipati et al. J A C C V O L . 7 0 , N O . 2 3 , 2 0 1 7

Catheter Ablation of VT in Structural Heart Disease D E C E M B E R 1 2 , 2 0 1 7 : 2 9 2 4 – 4 1

2926

Ventricular arrhythmias, including frequent PVCsand VT, are the major manifestation of disease andcause SCD. The PVCs and VT are typically left bundlebranch block morphology and may have an inferior(similar to idiopathic outflow tract VT) or superioraxis. Sustained VT occurs in approximately one-thirdof 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).

HYPERTROPHIC CARDIOMYOPATHY

In high-risk individuals with hypertrophic cardio-myopathy (HCM) receiving an ICD for either primary orsecondary prevention, the overall rate of ICD inter-vention is 5.5%/year (primary prevention 3.6%/year;secondary prevention 10.6%/year) (30). MonomorphicVT accounts for 38% of episodes (31). Although mono-morphic VT may occur in any HCM patient withmyocardial scar, the subgroup of patients with LV an-eurysms seems to be at higher risk (32–36). Mortalityrates are similar in those with and without LV

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 patientswith LV aneurysms and primary prevention ICDsexperience monomorphic VT, and another 3.7% expe-rience VF during w4.5 years of follow-up (33). ThemechanismofmonomorphicVT in thesepatients is alsoscar-related re-entry and is amenable to catheter abla-tion (32–36).

CARDIAC SARCOIDOSIS

Sarcoidosis is a systemic inflammatory process result-ing in noncaseating granulomas. Although mostcommonly associated with pulmonary involvement,myocardial involvement is frequent and is reported tobe present in up to 25% of patients on autopsy (37).Clinical manifestations are often absent, althoughconduction 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


2927

promote an inflammatory process, and later exert ananti-inflammatory effect and tissue scarring (39). Dueto progressive inflammation and a complex underlyingsubstrate, ventricular arrhythmias may have severalmechanisms, including abnormal automaticity, trig-gered activity, or scar-related re-entry (40). CMR withdelayed enhancement and 18F-fluorodeoxyglucose-positron emission tomography are useful to define theextent of myocardial scar and inflammation, respec-tively.When inflammation is present, the combinationof immunosuppressive therapy and antiarrhythmicdrugs may decrease VT recurrence. However, whenthese fail, catheter ablation is feasible (41,42).

CHAGAS CARDIOMYOPATHY. Chagas disease is causedby the flagellate protozoan parasite Trypanosomacruzi and is transmitted by hematophagous tri-atomine insect vectors. It is endemic to Latin Amer-ican countries, but is also prevalent in nonendemicareas due to population migration (43). One-third ofinfected individuals will develop chronic symptom-atic disease, with cardiac involvement being the mostfrequent and severe manifestation (44). Chronicmyocarditis affects all cardiac chambers and mayresult in conduction system abnormalities, segmentalwall motion abnormalities, diastolic dysfunction, andLV systolic dysfunction. Wall motion abnormalities,resulting from myocardial scarring, most frequentlyaffect the inferolateral and apical LV segments, oc-casionally culminating in apical aneurysms. Mono-morphic VT due to scar-related re-entry can arisefrom any scar location, but the inferolateral segmentis the most common source, accounting for w80% ofVTs (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 VTcircuits, Sosa et al. (47,48) first described the tech-nique of pericardial mapping using a percutaneoussubxyphoid approach. Long-term success rates ofcatheter ablation in Chagas patients are markedlyimproved with the incorporation of epicardial map-ping and ablation (46).

MANAGEMENT

ICDs AND ANTIARRHYTHMIC DRUGS. Numerousmulticenter randomized clinical trials support ICDsas the principal treatment modality for the primaryand secondary prevention of SCD in patients withstructural heart disease (49–51). Although the mor-tality benefit has been consistent in patients withcoronary artery disease, the benefit of primary pre-vention ICDs in nonischemic cardiomyopathy hasrecently been questioned. Current guidelines

supporting ICD implantation in this population arelargely based on the SCD-HeFT (Sudden CardiacDeath in Heart Failure Trial), COMPANION (Compar-ison of Medical Therapy, Pacing, and Defibrillation inHeart Failure), and DEFINITE (Defibrillators in Non-Ischemic Cardiomyopathy Treatment Evaluation)studies, which together demonstrated reduced mor-tality (52–54). In the more recent DANISH (DanishStudy to Assess the Efficacy of ICDs in Patients withNon-ischemic Systolic Heart Failure on Mortality),the primary endpoint of all-cause mortality wassimilar between groups randomized to ICD or usualclinical care (hazard ratio [HR]: 0.87; 95% confidenceinterval [CI]: 0.68 to 1.12; p ¼ 0.28) (55). However,1) there was still a significant reduction of SCD withthe ICD (HR: 0.50; 95% CI: 0.31 to 0.82; p ¼ 0.005);and 2) a pooled analysis of 6 primary prevention trialsdemonstrated a statistically significant 23% riskreduction 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 longVT detection interval and a high VF detection rate todecrease rates of overall ICD therapy (antitachycardiapacing and shocks), inappropriate therapy, andpotentially, mortality (57,58).

Beta-blockers, if not contraindicated, are recom-mended as they decrease mortality following VT/VFand in patients with heart failure and reduced leftventricular function (59). They are ineffective as soletherapy at decreasing VT/VF recurrence, but thecombination of amiodarone and beta-blockerssignificantly decreases the rate of recurrent ICDshocks compared with either sotalol or beta-blockersalone (60). However, in a meta-analysis, anti-arrhythmic drugs did not decrease mortality, butwere associated with a 34% reduction in rates ofappropriate ICD therapies and a 70% reduction ininappropriate ICD therapies (61). The reduction in VTwas largely driven by studies involving amiodarone,which interestingly, is itself associated with higherall-cause mortality in ICD recipients. Additionally,adverse drug reactions related to amiodarone occur inapproximately 30% of patients, requiring alternativedrug therapy or catheter ablation (62).

Despite these limitations, for VT patients withstructural heart disease, the combination of beta-blocker and amiodarone is the typical drug regimenfor VT/VF suppression. Mexiletine is often added forbreakthrough VT/VF. Other medications such assotalol or dofetilide are typically secondary options.Thus, for patients with recurrent ICD therapies,antiarrhythmic drugs are useful to decrease VT/VFrecurrence, but do not alter mortality; indeed, amio-darone may increase mortality.



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CATHETER ABLATION

INDICATIONS FOR CATHETER ABLATION. For patientswith structural heart disease, catheter ablation as soletherapy is not indicated for the primary or secondaryprevention of SCD. Rather, it is employed as adjunc-tive therapy to ICD implantation for secondary pre-vention when antiarrhythmic drugs are eitherineffective or not desirable. Four multicenter, ran-domized clinical studies have evaluated the adjunc-tive role of catheter ablation in addition to ICDs forthe secondary prevention of ventricular arrhythmias.The SMASH-VT (Substrate Mapping and Ablation inSinus Rhythm to Halt Ventricular Tachycardia) studyrandomized patients with prior MI presenting withspontaneous VT/VF to ICD implantation alone or incombination with catheter ablation (63). Patientstaking class I or III antiarrhythmic drugs wereexcluded. Catheter ablation resulted in a 65% reduc-tion in the rate of appropriate ICD therapy. Similarly,the VTACH (Ventricular Tachycardia Ablation inCoronary Heart Disease) study randomized patientswith prior MI, LVEF #50%, and hemodynamicallystable VT to ICD implantation or ICD implantationand ablation (64). Amiodarone was used in 35% ofpatients in each group at the time of randomization.At w2 years, the primary endpoint of time to firstrecurrence of VT or VF was significantly longer withthe ablation group versus control group (median18.6 months vs. 5.9 months). The freedom from VT/VFwas 47% in the ablation group and 29% in thecontrol 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 primaryendpoint of time to first VT/VF recurrence in post-MIpatients with LVEF #40% and hemodynamically un-stable VT (65). However, ablation did result in a >50%reduction in total ICD interventions. Antiarrhythmicdrug (class I or III) use was approximately 30% in bothgroups at time of enrollment.

Recently, the VANISH (Ventricular TachycardiaAblation versus Escalated Antiarrhythmic Drug Ther-apy in Ischemic Heart Disease) trial evaluated therelative roles of catheter ablation versus escalatingantiarrhythmic drug therapy in post-MI ICD patientswith recurrent VT despite receiving class I or III drugs,a typically encountered clinical situation (62). Thecomposite primary endpoint of death, VT storm, orappropriate ICD shock was reduced by 28% with abla-tion (HR: 0.72; 95% CI: 0.53 to 0.98; p ¼ 0.04). None ofthe individual components of the primary endpointwere significantly different between groups, likelybecause of the relatively small sample (n ¼ 259).

It should be noted that in these 4 trials, there weredifferences in ICD programming and how VT/VF re-currences were defined that may partially account fordifferences in outcomes. Additionally, none of the 4aforementionedmulticenter randomized clinical trialssupport catheter ablation for the reduction ofmortality.

In patients with structural heart disease, the 2009European Heart Rhythm Association and HeartRhythm Society Expert Consensus on CatheterAblation of Ventricular Arrhythmias recommendscatheter ablation for: 1) patients with sustainedmonomorphic VT that recurs despite antiarrhythmicdrugs or when drugs are not tolerated or desired;2) control of incessant sustained monomorphic VT orVT storm that is not due to a transient reversiblecause; 3) bundle branch re-entrant or interfascicularVT; 4) frequent PVCs, nonsustained or sustained VTin the setting of ventricular dysfunction; and5) recurrent sustained polymorphic VT and VF that isrefractory to antiarrhythmic therapy and thought tobe secondary to a trigger that is amenable for abla-tion (66). Additionally, catheter ablation is consid-ered for sustained monomorphic VT despite therapywith class I/III antiarrhythmic drugs, as an alterna-tive to amiodarone in patients with prior MI andLVEF >30%, and as an alternative to antiarrhythmicdrugs for hemodynamically tolerated sustainedmonomorphic VT due to prior MI and LVEF >35%.The 2014 European Heart Rhythm Association/HeartRhythm Society/Asia Pacific Heart Rhythm SocietyExpert Consensus on Ventricular Arrhythmias andthe 2015 European Society of Cardiology (ESC)guidelines for the management of ventricular ar-rhythmias provide additional and slightly differentrecommendations regarding the role of catheterablation (67,68). These various recommendations areconsistent with our approach, summarized in theCentral Illustration.OVERVIEW OF CATHETER ABLATION. Catheterablat ion techn iques . The general approach to cath-eter ablation of VT involves the characterization oftarget VTs, delineation of the arrhythmic substrate,and radiofrequency ablation of the arrhythmic tissue.Target VTs include all clinically occurring VTs andthose induced with programmed stimulation. Typi-cally, programmed ventricular stimulation is per-formed at 2 drive cycle lengthswith up to 3 extrastimulidelivered at progressively shorter coupling intervals at2 ventricular locations. When VT is induced, pace-termination or electrical cardioversion is performed,and programmed stimulation is continued until thesame VT is repeatedly induced or multiple electrical

CENTRAL ILLUSTRATION Role of Catheter Ablation in the Management of Patients With Structural Heart Disease

Structural Heart Disease

Sustained PMVT or VFdue to PVC Trigger

Frequent PVCs or NSVTwith LV Dysfunction Sustained MMVT

SingleEpisode

RecurrentVT

IncessantVT or VT

Storm

Normal LV Function onReassessment

ICD if LVEF≤35%

ICD NotIndicated

AADs

ICD

AADs

AADs

Failure

Failure

ICD

ICDYesNo

ConsiderVT Suppression

Catheter Ablation

Catheter Ablation

AADsFailureCatheter

Ablation

Catheter Ablation

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.


2929

cardioversions are required. For each VT, the 12-leadECG morphology, the rate (or cycle length), bundlebranch block morphology, axis, precordial transition,and the hemodynamic effect are all recorded. This notonly helps localize the VT exit site, but also helpsdetermine the ablation strategy as described in thefollowing text.

The myocardial scar is identified using a 3-dimensional (3D) electroanatomic mapping systemthat allows: 1) spatial localization of a mapping cath-eter; 2) generation of a 3D anatomic representation ofthe ventricle that is color-coded based on electrogramvoltage amplitude recorded from the mapping cath-eter to differentiate normal myocardium from scar orborder zone tissue; and 3) cataloging of myocardialchannels and potential VT circuit isthmus sitesidentified 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 bipolarvoltage <0.5 mV, and border zone tissue by bipolarvoltage of 0.5 to 1.5 mV (69). As previously described,myocardial channels responsible for re-entrant VTreside in the border zone. These channels havecharacteristic bipolar electrograms and can be classi-fied as fractionated electrograms or as late (or iso-lated) potentials. Fractionated electrograms havemultiple components without an isoelectric segmentand an amplitude #0.5 mV, a duration $133 ms,and/or an amplitude/duration ratio #0.005. A late orisolated potential occurs after the QRS complex and isseparated from the ventricular electrogram by anisoelectric interval of >20 ms (Figure 1) (70,71). Limi-tations of voltage mapping include variation of



2930

bipolar and unipolar amplitudes due to wave frontdirection, electrode size and spacing, as well asannotation of multiple component signals to thelargest peak.

Sites demonstrating late or isolated potentialscorrelate with critical portions of the VT circuitisthmus and are desirable targets for ablation (72,73).Fractionated and late/isolated potentials may be un-derappreciated during sinus rhythm andmaymanifestonly with ventricular pacing. In sinus rhythm, theseelectrograms may demonstrate superimposed localelectrical activity and far-field ventricular activityinscribed during the QRS complex. Ventricular pacingmay cause a delay of the local electrogram and causeseparation from the far-field component. Theseabnormal electrograms, together with fractionatedand late/isolated potentials, are broadly classified aslocal abnormal ventricular activity (LAVA) and havealso been shown to be desirable ablation targets for VT(74). However, it should be noted that zones of slowconduction or deceleration may be more functionallyrelevant than the latest activated regions (75).

After VT induction and delineation of thearrhythmic substrate, ablation strategies typicallyinclude a combination of entrainment mapping,activation mapping, pace mapping, and substratemodification for VT. Certain sites demonstratingfractionated electrograms, late/isolated potentials, orLAVA in sinus rhythm may show diastolic electro-gram activity during VT. However, not all of theselocations will be critical for maintaining VT; they maysimply represent diastolic activity due to passiveactivation (Figure 2). The most reliable method fordetermining the relevance of a channel of activationis to utilize entrainment maneuvers during VT (76). Adetailed description of entrainment is beyond thescope of this paper; briefly, it involves overdrivepacing of VT from a site to determine whether thatsite is a critical component of the tachycardia circuitor is a bystander site. Targeting of the sites that fulfillentrainment criteria for VT circuit isthmus sites has ahigh incidence of terminating VT (Figure 3).

Activation mapping involves the identification ofthe earliest site of electrical activation in a cardiacchamber in comparison to an arbitrary referenceelectrogram during VT. This information can be colorcoded and recorded on a 3D electroanatomic map sothat the earliest site of local electrical activation canbe identified. This is particularly useful for focal VTthat has a single earliest site with centrifugal activa-tion away from that location. Because electrical ac-tivity is continuous, activation mapping in re-entrantVT is not useful to delineate early and late activation;however, it can be used to identify VT exit sites along

the scar border and identification of diastolic corri-dors during VT. These areas of diastolic activationmay or may not represent critical components of theVT circuit (isthmus vs. bystander sites) but are oftentargeted for ablation.

Entrainment and activation mapping cannot beperformed in the presence of hemodynamically un-stable VT, which is reported to occur in 69% of pa-tients with ischemic cardiomyopathy undergoing VTablation (9). After scar delineation in sinus rhythm,pace mapping is a methodology utilized to targetthese unstable VTs without requiring VT induction.This involves pacing along the scar periphery tomatch the paced 12-lead ECG morphology with theclinical VT morphology, thereby identifying the VTexit sites. Pacing adjacent to the exit site, but furtherwithin the scar, may identify potential VT isthmussites, characterized by latency between the pacingstimulus and the paced QRS (stimulation to QRS in-terval >80 ms) (72,77,78). Alternatively, substratemodification of the scar can be performed that targetsall fractionated/late potentials and LAVA.

The traditional approach to ablation of scar-relatedVT has involved using a combination of entrainment/activation mapping for hemodynamically toleratedVT and pace mapping and substrate modification forunstable VT. We previously demonstrated that it ispossible to map otherwise hemodynamically unstableVT during tachycardia with the use of percutaneousleft ventricular assist devices (LVADs) (79,80). Thesedevices maintain end-organ perfusion during pro-longed periods of VT, allowing a longer time fordetailed entrainment/activation mapping, requiringfewer terminations for hemodynamic instability, andresulting in more VT terminations with ablation.However, the observational studies are non-randomized, and are thus unable to demonstratelong-term outcome benefits such as mortality reduc-tion or VT suppression. In our experience, these de-vices decrease post-procedure heart failure and maybe of potential benefit during VT ablation in patientswith New York Heart Association functional class $IIIheart failure, severe LV dysfunction, or electricalstorm, as these types of patients are at high risk foracute 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 preemptivelyin high-risk patients undergoing VT ablation or as abailout measure when intraprocedural hemodynamicdeterioration occurs (83). In these patients, ECMOwas not only safe, but also allowed prolonged VT

FIGURE 2 Myocardial Scar and Mechanism of Re-Entrant VT

NormalMyocardium

Border ZoneScar

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

MAP *

A

B

*

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

MAPBorder ZoneScar

NormalMyocardium

(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.


2931

activation mapping (median 30 min) and a high rateof VT termination with ablation (81% of patients). Inunstable patients, ECMO can bridge unstable patientsto permanent LVAD or heart transplantation (83).

Bundle branch re-entrant VT typically occurs indilated cardiomyopathy but can also be seen in otherdiseases with underlying His-Purkinje disease (84).

The rate is often rapid and poorly tolerated hemo-dynamically. The mechanism is macro–re-entry andinvolves both the right and left bundle branches,ventricular myocardium, and the His bundle. Leftbundle branch block morphology during VT is morecommon than a right bundle branch block pattern.Typically, the retrograde limb is the left bundle

FIGURE 3 Catheter Ablation of Scar-Related VT in a Patient With Prior Inferior Wall Myocardial Infarction

III

IIIaVRaVLaVF

V1V2V3V4V5

V6

MAP

III

III

LEFT LATERAL/CAUDAL

A D

B C

INFERIOR INFERIOR

Apex

MV

Lateral

Septum

Apex

aVRaVLaVF

V1V2V3V4V5

V6

MAPTermination* *

(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.



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branch and the antegrade limb is the right bundlebranch. 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 bundlebranch block in sinus rhythm, the risk of completeheart block is increased, and ablation with elimina-tion of left bundle branch retrograde conduction ispreferable.

The technique for catheter ablation of polymorphicVT/VF due to PVC triggers and of PVCs resulting in leftventricular dysfunction in patients with structural

heart disease is similar to that in patients with struc-turally normal hearts, andwas reviewed in part I of thisseries.Epicard ia l ab lat ion . Although most VT circuitsin post-MI patients are subendocardial, a third ofpatients may require epicardial ablation for mid-myocardial or subepicardial circuits (85). Further-more, as previously mentioned, epicardial mapping isuseful in DCM VT, particularly in ARVC/D and Chagasdisease, due to preponderance of midmyocardial andsubepicardial scar. The epicardial space is accessedusing a percutaneous subxyphoid puncture approachin those patients without prior cardiac surgery, and

FIGURE 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.


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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 epicardialapproach. The presence of midmyocardial or sub-epicardial scar on CMR identifies patients that arelikely to require epicardial mapping for successfulabolition of VT (25). The use of pre-procedural CMRhas been shown to be independently associated withimproved procedural success and the compositeendpoint of VT recurrence, heart transplantation, ordeath in DCM patients undergoing VT ablation (88).

Patients that should be considered for epicardialmapping include those with: a failed prior ablation,VT unrelated to coronary artery disease (i.e., DCM,ARVC/D, HCM, and Chagas cardiomyopathy, wherethere is a higher likelihood of subepicardial scar), aCMR suggesting midmyocardial or epicardial scar, oran ECG suggestive of an epicardial exit (Figures 4and 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 slowupstroke/downstroke of the initial part of the QRScomplex during VT (a pseudo-delta wave). Althoughthese criteria are widely used, their discriminatory

power in the setting of myocardial scar has beenquestioned (92,93).OUTCOMES OF CATHETER ABLATION. The results ofcatheter ablation in post-MI patients are reasonable,with 1-year recurrence rates between 23% and 49%,and with many patients remaining on antiarrhythmicdrugs (94–96). These results were obtained withmostly traditional VT mapping techniques, such asentrainment/activation mapping of hemodynamicallystable VT and pace mapping, and limited substrateablation for poorly tolerated VT. Recently, alternatepredominantly substrate-based ablation strategiestargeting all of the arrhythmogenic myocardium(fractionated/late potentials and LAVA) in sinusrhythm have been evaluated (74,85,97–99). Thesestrategies have yielded higher success rates when allidentifiable myocardial channels were targeted. Inthe VISTA (Ablation of Clinical Ventricular Tachy-cardia Versus Addition of Substrate Ablation on theLong Term Success Rate of VT Ablation) trial (100),ischemic cardiomyopathy patients with hemody-namically tolerated VT were randomized to targetclinical VTs using entrainment, activation, and pacemapping versus an extensive substrate-based abla-tion strategy targeting all abnormal electrogramswithin the scar. The primary endpoint of VT

FIGURE 5 Catheter Ablation of VT in HCM With Midcavitary Obstruction and Apical Aneurysm

III

C

BA

IIIaVRaVLaVF

V1

V2V3V4V5

V6VT Termination

9.0 sMAP 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.



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recurrence at 12 months was 48.3% in the clinical VTablation group and 15.5% in the substrate ablationgroup (log-rank p < 0.001). Substrate ablation wasassociated with a 67% lower risk of VT recurrencecompared with clinical VT ablation (HR: 0.33; 95% CI:0.13 to 0.81; p ¼ 0.014). There were no differences inmortality 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 ofintramural substrate and infrequent substrate

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, thesuccess rates of catheter ablation have markedlyimproved (107–112). A large, single-center study re-ported a 71% rate of freedom from recurrent VTfollowing multiple procedures during a mean follow-up of nearly 5 years (112). There are very few reportedHCM and cardiac sarcoidosis patients treated withcatheter ablation; however, catheter ablation, oftenusing a combined endocardial/epicardial approach,


2935

appears to be reasonably efficacious and safe inthe treatment of drug-refractory VT in these patients(32–36,41,42).

Although catheter ablation has not been proven toimprove mortality, there is evidence that a successfulablation is associated with not only a higher rate offreedom from VT, but also improved survival. Aretrospective analysis of outcomes of VT ablationfrom high-volume centers demonstrated that freedomfrom recurrent VT after catheter ablation is stronglyassociated with a significant reduction in all-causemortality, independent of ejection fraction and heartfailure status (95). A meta-analysis of 8 cohort studieswith 928 post-infarction VT patients demonstratedthat complete noninducibility after ablation wasassociated with a significant reduction in recurrentventricular arrhythmias when compared with partialsuccess (odds ratio [OR]: 0.49; 95% CI: 0.29 to 0.84;p ¼ 0.009) or procedure failure (OR: 0.10; 95% CI: 0.06to 0.18; p < 0.001) (113). Importantly, noninducibilitytranslated 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 cardiomyopathypatients, noninducibility was associated with a 35%reduction in mortality (114). A similar finding has beenreported in dilated cardiomyopathy patients (103).However, it should be recognized that all of thestudies indicating improved survival with successfulVT ablation (i.e., noninducibility) are nonrandomized.It is also important to note that early referral of pa-tients for catheter ablation is associated withimproved freedom from VT compared with laterreferral when arrhythmic burden and substrateseverity are higher (115).

Major procedure-related complications may occurin w7% of patients (9,62,95,116). Cardiac perforationoccurs in 1.5%, major vascular injury in 2.3%, anddeath in up to 3%. Other complications include un-controllable VT in up to 2.6%, stroke or transientischemic attack in 0.5%, heart block in 0.9%, andcoronary artery injury in 0.2%. Acute hemodynamicdecompensation, defined as persistent hypotensiondespite vasopressors requiring mechanical support ordiscontinuation of the procedure, is reported to occurin 11% of patients and portends increased mortality(81). Although these risks are not inconsequential, itis important to remember that these patients have alife-threatening condition that, if untreated, is likelyto culminate in mortality.

To identify patients at highest risk for hemodynamicdecompensation, the PAAINESD risk score (Pulmonarydisease, Age >60 years, general Anesthesia, Ischemic

cardiomyopathy, New York Heart Association func-tional class III or IV, Ejection fraction <25%, VT Storm,Diabetes mellitus) has been developed (81). This riskscore may be useful to not only prospectively identifyhigh-risk patients likely to benefit from hemodynamicsupport during ablation, but also identify patients thatshould undergo multidisciplinary evaluation (i.e.,heart failure and cardiothoracic surgery) for perma-nent LVAD or heart transplantation in the case thathemodynamic decompensation should occur during orfollowing VT ablation. The reported 1-year mortalityrate following VT ablation is 18%, with a primarymechanism of death of either recurrent VT (37.5%) orrefractory heart failure (35%) (9). Early mortality(#30 days) following VT ablation occurs in 5% of pa-tients, with more than one-half of patients dyingbefore hospital discharge (116). The primary mecha-nism of early mortality is also refractory VT oradvanced heart failure. Predictors of early mortalityinclude LVEF, chronic kidney disease, presentationwith VT storm, and presence of unmappable VTs (116).

The outcomes of patients with structural heartdisease undergoing ablation of PVCs resulting in LVdysfunction and polymorphic VT/VF is more favor-able (reviewed earlier in Part I).

ADJUNCTIVE THERAPIES AND

FUTURE DIRECTIONS

The efficacy of catheter ablation is occasionallylimited by the presence of intramyocardial VT circuitsunreachable with standard irrigated radiofrequencyablation catheters. In these situations, ancillarytechniques 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 injectionof ethanol via an occlusive balloon catheter tocause intramural myocardial necrosis. This tech-nique, although useful for the eradication ofintramyocardial VT, is limited by dependence on acoronary anatomy with the requisite distribution(117) (Figure 6).

2. Bipolar radiofrequency ablation is performed be-tween 2 ablation catheters positioned on opposingventricular walls adjacent to the intramyocardialVT circuit. Bipolar ablation produces larger andmore transmural lesions compared with standard(unipolar) ablation performed sequentially onopposing sides of the target tissue and can be usedto terminate VT when standard methods fail (118)(Figure 7).

3. Intramural needle ablation catheters are designedto allow a needle electrode to be advanced into the

FIGURE 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.



2936

ventricular wall to create large intramural radio-frequency lesions (119,120). Although promising forthe treatment of intramural VT circuits, thesetechniques create larger lesions and may increasethe risk of complications including cardiac perfo-ration, atrioventricular block, and worsening LVfunction. Although these techniques are useful forthe termination of any given VT, none has beenshown to improve long-term freedom from VT. Assparse data exist, the efficacy and safety of bipolarcatheter ablation and intramural needle ablationare being further evaluated in nonrandomizedsingle and multicenter studies (Bipolar VentricularTachycardia [VT] Study, NCT02374476; IntramuralNeedle Ablation for Ventricular Tachycardia,NCT02799693; Intramural Needle Ablation for theTreatment of Refractory Ventricular Arrhythmias,NCT03204981).

Stereotactic radioablation is commonly used tononinvasively treat solid tumors, and has recentlybeen considered for the treatment of ventriculartachycardia (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 targetarrhythmogenic substrate is identified using imaging(i.e., CMR, computed tomography, and positron-emission tomography). The mechanism of tissuedeath is apoptosis and microvascular injury ratherthan thermal as with radiofrequency ablation, andtypically has a delayed manifestation (days tomonths). Clinical data is very limited, but ongoingmulticenter trials will provide more insight into thesafety and efficacy of this treatment modality.

Autonomic modulation targets the known centralrole that the autonomic nervous system plays in theinitiation andmaintenance of ventricular arrhythmias.The most common neuromodulation method is left orbilateral cardiac sympatheticdenervation (CSD),whichinvolves the resection of the lower third of the stellateganglia, T2 to T4 thoracic ganglia, and the nerve ofKuntzwhen present (123,124). In a recent retrospectivemulticenter study of 121 patients with refractory VT orVT storm, CSD was associated with a 1-year freedomfrom sustained VT or ICD shocks of 58%, and freedomfrom ICD shocks, sustained VT, death, or heart trans-plantation of 50% (124). Bilateral CSD was superior toleft CSD. Another method of neuromodulation, renalsympathetic denervation, is conceptually attractive,but is only supported by sparse data.

https://clinicaltrials.gov/ct2/show/NCT02374476



FIGURE 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.


2937

CONCLUSIONS

Catheter ablation of ventricular tachycardia in pa-tients with structural heart disease can significantlyreduce the incidence of recurrent ventricular ar-rhythmias. It is best used as an adjunct to ICDs, and asan alternative or adjunct to antiarrhythmic drugs.Certain patients with left ventricular dysfunction dueto frequent ventricular ectopy benefit from catheterablation as a primary treatment strategy, becauseventricular dysfunction may be reversible, therebyobviating the need for ICD therapy.

Although catheter ablation reduces recurrent ven-tricular arrhythmias, randomized controlled trialspowered to examinemortality reduction have not beenperformed. However, observational studies indicatethat successful catheter ablation reduces mortality.Earlier referral for VT ablation is strongly associatedwith improved outcomes when compared to laterreferral, where arrhythmic burden and substrateseverity are higher. Overall, catheter ablation in thispopulation has an acceptable risk, but patients

presenting with VT storm, advanced heart failure withseverely reduced LV function, and certain othercomorbidities are at increased risk for procedure-related hemodynamic decompensation; they maybenefit from percutaneous hemodynamic supportduring the procedure. These patients should undergopre-procedure optimization of heart failure and amultidisciplinary evaluation for advanced therapiesshould hemodynamic decompensation occur. Therates of ventricular arrhythmia recurrence are signifi-cant, partially due to the inability to ablate VT circuitsthat are present deep within the myocardium. In thesesituations, 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 SinaiMedical Center, One Gustave L. Levy Place, Box 1030,New York, New York 10029. E-mail: [email protected].

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KEY WORDS catheter ablation, PVCs,structural heart disease, ventricularfibrillation, ventricular tachycardia

















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Catheter Ablation of Ventricular Tachycardia in Structural ... · electrical conduction through the border zone pre-disposes to re-entrant VT (1–4). Additionally, there are adaptive