catheter ablation of ventricular tachycardia in ischaemic and non

REVIEW

Clinical update

Catheter ablation of ventricular tachycardiain ischaemic and non-ischaemic cardiomyopathy:where are we today? A clinical reviewErik Wissner1, William G. Stevenson2, and Karl-Heinz Kuck1*

1II. Medizinische Abteilung, Asklepios Klinik St Georg, Lohmuehlenstrasse 5, 20099 Hamburg, Germany; and 2Cardiovascular Division, Brigham and Women’s Hospital,75 Francis Street, Boston, MA 02115, USA

Received 21 August 2011; revised 17 December 2011; accepted 6 January 2012; online publish-ahead-of-print 11 March 2012

According to the current guidelines, patients with ischaemic cardiomyopathy (ICM) or non-ischaemic cardiomyopathy (NICM) at risk forsudden cardiac death should undergo implantation of an implantable cardioverter-defibrillator (ICD). Although ICDs effectively terminateventricular arrhythmias, the arrhythmogenic substrate remains unchanged or may progress over time, resulting in recurrent ICD shocks.Defibrillator shocks increase mortality and worsen quality of life. Evidence from two prospective randomized trials on outcome in patientswith ischaemic heart disease undergoing catheter ablation for ventricular tachycardia (VT) suggests that ablation prevents recurrence of VTand decreases the number of ICD shocks. This review will highlight the recent progress made in the ablative treatment of VT in patients withICM and NICM.- - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - - -Keywords Ventricular tachycardia † Ischaemic cardiomyopathy † Non-ischaemic cardiomyopathy † Radiofrequency ablation

† Catheter ablation † Clinical outcome † Implantable cardioverter-defibrillator

IntroductionCatheter ablation of ventricular tachycardia (VT) has made signifi-cant strides over recent years with new evidence from prospectiverandomized trials on outcome in patients with ischaemic heartdisease. Implantable cardioverter-defibrillators (ICDs) are currentlythe mainstay of treatment for patients with ischaemic cardiomyop-athy (ICM) or non-ischaemic cardiomyopathy (NICM), who are atrisk for sudden cardiac death due to VT.1,2 However, ICDs effective-ly terminate VT, but do not prevent VT episodes. The arrhythmo-genic substrate remains unchanged or may progress over time,resulting in new or increasingly frequent episodes of VT in a consid-erable number of patients. Defibrillator shocks increase mortalityand worsen quality of life.3 –5 b-Blocker therapy in combinationwith amiodarone reduces ICD shocks for some patients; however,amiodarone has significant side effects, resulting in drug discontinu-ation in nearly 25% of the patients.6 Catheter ablation now has animportant role to control incessant VT and to reduce or prevent re-current episodes of sustained VT.7 –12 This review will focus on theprogress that has been gained over recent years in the ablative treat-ment of VT in patients with structural heart disease.

The importance of ventriculartachycardia types, substrates,and the 12-lead surfaceelectrocardiogramThe majority of patients who have recurrent episodes of sustainedVT have an arrhythmia substrate defined by areas of ventricularscar. Scars can be due to prior myocardial infarction in thosewith coronary artery disease, or replacement fibrosis in non-ischaemic heart diseases, or surgical incisions, as after repair of tet-ralogy of Fallot. Surviving myocyte bundles within the scars charac-terized by diminished cell coupling and interstitial fibrosis promoteslow conduction and create regions of anatomical or functionalconduction block causing reentry.13 The reentry circuit includesan isthmus of slow conduction. The exit site of the criticalisthmus gives rise to the QRS complex and is often the initialtarget during catheter ablation. The isthmus may span several cen-timetres.14 Furthermore, the reentry circuit needs to be appre-ciated as a complex three-dimensional construct that can involvethe endocardium, mid-myocardium, or epicardium.15

* Corresponding author. Tel: +49 40 1818 852305; Fax: +49 40 1818 854444, Email: [email protected]

Published on behalf of the European Society of Cardiology. All rights reserved. & The Author 2012. For permissions please email: [email protected]

European Heart Journal (2012) 33, 1440–1450doi:10.1093/eurheartj/ehs007

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Ventricular tachycardia due to scar-related reentry is usuallymonomorphic, with each QRS complex resembling the precedingand following QRS. In monomorphic VT, the sequence of ventricu-lar depolarization is the same from beat to beat. The QRS morph-ology of VT is determined by the location of the scar and thelocation of the reentry circuit within the scar, specifically theexit region where the reentry wavefronts propagate away fromthe scar to depolarize the ventricles. Typically, multiple VT morph-ologies can be induced in the same patient. Multiple VTs may sharethe same isthmus with different exit sites or depend on differentisthmi within the same scar or indicate the presence of differentreentry circuits in different regions of scar (Figure 1). In somepatients, one monomorphic VT may initiate a second monomorph-ic VT causing more than one distinct QRS configuration during asingle VT episode, known as pleomorphic VT.16 Ventricular tachy-cardias that occur spontaneously are commonly referred to as clin-ical VTs. Programmed ventricular stimulation may initiate othermorphologies of VT, of less certain clinical relevance, which maynot necessarily occur spontaneously.

Polymorphic VTs have a continually changing QRS morphology,indicating a changing sequence of ventricular activation. Althoughventricular scar may be present, these arrhythmias are often asso-ciated with acute myocardial ischaemia, inherited ion channel ab-normalities, or ventricular hypertrophy; and a fixed structuralsubstrate, such as scar, is not required. Polymorphic VTs are lesslikely to have an identifiable substrate that can be targeted for

ablation and warrant a different set of diagnostic and therapeuticconcerns.

From these considerations, it is clear that electrocardiographic(ECG) recordings of the spontaneous VT are very helpful inguiding evaluation and therapy. Documentation of the spontan-eously occurring clinical VT on the 12-lead surface ECG shouldalways be sought if possible. The QRS morphology can serve asa guide during the mapping and ablation procedure to recognizeclinical VTs and suggest the location of the VT substrate. Rightbundle branch block morphology in lead V1 suggests a left ven-tricular (LV) origin, while left bundle branch block morphology(dominant S-wave) indicates an exit site from the right ventricleor interventricular septum. A superior axis is expected for sitesemanating from the inferior ventricular wall. Cranial sitesproduce an inferior axis. Deep S-waves in the precordial leadsV3 and V4 indicate an apical exit site, while dominant R-wavespoint towards an exit along the base of the ventricle.17

In patients with non-ischaemic cardiomyopathy (NICM), theQRS morphology can also suggest whether epicardial ablation islikely to be required, which is helpful in advising the patientabout procedural risks and in optimizing the sequence ofmapping and the use of anticoagulation, which is ideally avoidedbefore attempting percutaneous epicardial access. Comparedwith endocardial VTs, those that originate from epicardial scar typ-ically have a wider QRS interval since the activation wavefront tra-verses from the epicardial to the endocardial layer before engagingthe rapidly conducting Purkinje system.18– 21,22 The presence of aQ-wave in lead I during VT is seen if local activation spreadsfrom the basal superior or apical superior epicardium to endocar-dium, while a Q-wave in the inferior leads suggests a site from thebasal inferior or apical inferior epicardium.20 These ECG criteriahave not been reliable in ischaemic cardiomyopathy (ICM).

Frequently, a 12-lead ECG of the clinical VT is not available inICD patients. The device promptly terminates VT with either anti-tachycardia pacing or shocks. In these cases, careful analysis ofstored ICD electrograms may facilitate morphological characteriza-tion of VT and, in some patients with ICM, can help recognize clin-ical VTs that are induced by programmed ventricular stimulationduring the procedure.23

Pre-procedural considerationsCardiac echocardiography should be performed in all patients pre-senting for ablation in order to rule out mobile LV thrombus. Sincecardioversion or defibrillation may be required during mapping andablation, in patients with concomitant atrial fibrillation, transoeso-phageal echocardiography should be performed to screen for leftatrial thrombus in patients who have not been chronically anticoa-gulated. If recent coronary vascular status is unknown or thepatient presents with polymorphic VT, coronary angiographyshould be performed. The presence of significant untreated coron-ary artery disease may limit mapping during tachycardia due tohaemodynamic compromise caused by myocardial ischaemia. Ifhaemodynamically unstable VTs are present or anticipated,general anaesthesia should be considered. In addition, the use ofa haemodynamic support system may facilitate proper mapping

Figure 1 A large area of left ventricular scar (yellow) inter-spersed with islands of dense scar (purple). Monomorphic ven-tricular tachycardia may utilize an area of slow conduction(zigzag line) juxtaposed between the mitral valve (MV) and anarea of dense scar (A, VT1). Of note, the QRS morphology willchange if activation traverses in the opposite direction utilizingthe same slow zone of conduction. Following ablation of VT1at an exit site, activation may proceed through a nearbyisthmus within the same scar incorporating parts of the previousreentry circuit (B, VT2). After successful ablation of VT2, add-itional tachycardias may occur utilizing different reentry circuitswithin the same scar (C, VT3 and VT4).

Catheter ablation of VT in ICM vs. NICM 1213dD

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and ablation and reduce risks of haemodynamic deterioration fromepisodes of VT during the procedure.24

Procedure techniquesProgrammed stimulation is performed in order to induce VT,confirm the diagnosis, assess the VT ECG morphology, and deter-mine whether VT non-inducibility may serve as the acute proced-ural endpoint (Figure 2). In the case of non-inducibility orinducibility of non-clinical VT, a substrate-based mapping and abla-tion approach may be chosen. If VT is haemodynamically unstable,it is immediately terminated using burst pacing or electrical cardi-oversion. Based on the location of the scar and the morphology ofthe VT, initial mapping then begins in either the right ventricle orLV, or the pericardial space. Endocardial LV mapping may be per-formed via a transseptal or a retrograde arterial approach. Damageto the aortic valve or coronary arteries is rare using a retrogradeapproach.7 If retrograde aortic access is difficult or impossible, as inpatients with significant peripheral vascular disease, aortic stenosis,or a mechanical aortic valve prosthesis, a transseptal approach isthe preferred route of access to the LV. A transseptal approachmay also be used concomitantly with a retrograde aortic accessto facilitate mapping in some patients. To date, no randomizedstudy has compared a retrograde transaortic with an anterogradetransseptal approach for LV mapping and ablation. Once LV accessis secured, unfractionated heparin should be administered to targetan activated clotting time of .250 s.

Epicardial ventricular tachycardiaablationEpicardial mapping and ablation is now commonly performed inexperienced centres when an epicardial VT is suspected. Inpatients with NICM and arrhythmogenic right ventricular cardio-myopathy/dysplasia (ARVC/D), endo- and epicardial mapping andablation are frequently performed in combination since thesepatients have a higher likelihood of epicardial involvement.25 Epi-cardial ablation is more frequently required in patients referredafter failed VT ablation.26

There are several unique aspects to epicardial mapping and ab-lation. Access to the epicardium is obtained via pericardial punc-ture from a subxyphoid approach, which allows placement of avascular introducer sheath into the pericardial space. Themapping and ablation catheter can then be inserted. Since anirrigated-tip ablation catheter (see below) is utilized for mappingand ablation, regular aspiration of epicardial fluid should be per-formed. Risks include pericardial bleeding (4.5%) that mayrequire emergent surgery, liver laceration (3%), and damage to epi-cardial coronary arteries (1.2%).26,27 Coronary angiography is oftenneeded to define the proximity of epicardial VT substrate to cor-onary arteries; and in some cases, overlying coronary arteries orproximity to the left phrenic nerve precludes ablation. Percutan-eous epicardial access is often not possible in patients who havepericardial adhesions, as are common after prior cardiac surgery.A surgical approach to ablation is an option for some of thesepatients. Some operators give prophylactic steroids following the

procedure in an attempt to decrease the likelihood of sterile peri-carditis that may be seen in up to 11% of the patients.26 Adhesionformation may interfere with repeat attempts at epicardial accessin up to 25% of the patients.26

Robotic mapping and ablationsystemsSystems that allow catheter manoeuvring from a console remotefrom the patient, with the use of magnetic fields to orient the cath-eter are a feasible alternative to conventional manual catheter ma-nipulation.28 It is hoped that procedure success will be lessdependent on individual operator skill, while fluoroscopy exposureto the patient and the operator is decreased. The soft-tipped mag-netic catheter is less likely to result in cardiac trauma, may reducecatheter-induced ventricular extrasystoles during mapping, andmay facilitate constant tissue contact during ablation. Evidence isaccumulating that remote-controlled ablation of VT is feasible;however, studies are needed to compare efficacy with manualcatheter mapping and ablation.29 Lastly, trials are underway toassess the feasibility of remote VT ablation using the Hansenrobotic system.

MappingScar-related VT circuits are often large. Ablation targets reentrycircuit isthmuses and their exits. The ability to identify and targetthe VT substrate has been greatly facilitated with the use ofmapping systems that permit accurate three-dimensional recon-struction of cardiac anatomy using point-by-point sampling. Theposition of the mapping catheter is traceable on the virtual map,reducing the need for fluoroscopy. Features of electrogram ampli-tude or timing can be colour-coded and displayed on the map(Figure 2B).30

When VT is not incessant, and particularly when induced VT isunstable, initial mapping of scar-related VT focuses on locating theabnormal myocardial substrate during stable sinus or paced rhythm(substrate mapping). When VT is stable, mapping is performedduring VT to delineate reentry circuit isthmuses and exits from ac-tivation mapping and entrainment mapping. Substrate mapping isalso often used in combination with mapping during VT in orderto minimize the time spent in VT, limiting the need for cardiover-sion and potential haemodynamic compromise.

Substrate and voltage mappingDefining the area of scar for substrate mapping necessitates anelectroanatomical mapping system (Figure 2B).30 Substratemapping may include voltage and pace mapping and registrationof characteristic electrogram features suggesting abnormal myocar-dium. Ablation can be guided by substrate mapping alone, but oftenidentifies a relatively large area of potential scar and reentry cir-cuits.31 Combining substrate mapping with short episodes of acti-vation and entrainment mapping, even in patients with unstable VT,will increase the likelihood of successful VT ablation.32

The amplitude (voltage) of an electrogram recorded by themapping catheter at each site is related to the mass of the

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underlying myocardium and is reduced when the myocardium isreplaced by scar. For bipolar recordings, an electrogram amplitudeof ,1.5 mV indicates a region of scar (Figure 3). A very low amp-litude of ,0.5 mV is commonly referred to as ‘dense scar’.30

Voltage maps correlate well with scars demonstrated by cardiacperfusion emission tomography using FDG uptake and delayedgadolinium enhancement on cardiac magnetic resonance (MR)imaging.33,34 This 1.5 mV threshold is very specific, but has

limited sensitivity, and fails to detect intramural or epicardialscar. Unipolar recordings have a deeper ‘field of view’, and unipolarvoltage mapping using a cut-off threshold of ,8.3 mV for abnor-mal tissue in dilated CM and ,5.5 mV in ARVC/D was able toidentify epicardial scar at the time of endocardial mapping, suggest-ing the need to proceed with epicardial ablation.35,36 With allvoltage maps, care must be taken to recognize low voltage dueto poor catheter tip-to-tissue contact, rather than true scar.

See figure legend on p. 1444.


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During substrate mapping, other abnormal electrogram featuresare noted and may be marked individually on the map. At areas ofslow conduction, asynchronous activation of myocyte bundles maygive rise to electrograms with multiple low-amplitude components,indicating abnormal conduction, as do late potentials, defined asdiscrete potentials separated from the main ventricular electro-gram, and that may occur after the QRS complex37 (Figure 4).These electrograms may indicate a reentry circuit isthmus.37,38

Pace mapping should then be performed in order to identifywhether these sites are critical to the reentry circuit.

Pace mappingThose sites in the scar, or along the scar border where pacing pro-duces the same QRS morphology as VT, are often in the exit oristhmus of the VT circuit (Figure 2C). Pace mapping shouldideally be performed at the tachycardia cycle length or at a cyclelength identical to the coupling interval of ventricular ectopy.However, a faster pacing cycle length increases the risk of inadvert-ent VT induction. Pacing at a faster cycle length or shorter couplinginterval will produce rate-dependent changes in the QRS morph-ology.39 A perfect pace map will replicate the VT QRS morphologyin all 12 surface ECG leads (12/12 match). Areas of electrically un-excitable scar can be marked as regions where pacing fails tocapture (unipolar pacing at 10 mA at a pulse width of 2 ms),which may form borders of the reentry circuit.40 Longstimulus-to-QRS intervals during pacing indicate regions of poten-tial slow conduction (Figure 2C ).

Mapping during ventricular tachycardiaIf VT is haemodynamically stable, mapping can be performedduring tachycardia. Activation sequence maps are created by plot-ting the electrogram timing relative to the QRS onset. The reentry

circuit exit and isthmus are depolarized prior to the QRS onset,giving rise to presystolic or diastolic electrograms.41 However,similar electrograms may also be recorded from bystander sitesthat are not an integral part of the reentry circuit.42 Recognitionof isthmuses can be accomplished by assessing the effect ofpacing at the site during VT (entrainment mapping) (Figure 2D).43

At times, an isthmus is recognized because simple mechanical pres-sure from the catheter terminates VT or a stimulus that does notappear to capture terminates VT.44,45

Catheter ablationAfter identification of a reentry circuit isthmus, ablation is per-formed, either during VT with observation for VT termination(Figure 2E) or during sinus rhythm. Radiofrequency ablation ismost commonly used for ablation. In contrast to ablation formost supraventricular tachycardias, large lesions are desirable forscar-related reentry circuits. Irrigated-tip RF ablation cathetersare commonly used in which saline flows through pores in the ab-lation electrode, cooling it to allow greater energy application withless risk of char formation to create deeper lesions. During irri-gated LV endocardial and epicardial ablation, power is set to30–50 W with a maximum temperature of 438C and a flush rateof 17–25 mL/min. Steam pops due to explosion of steam iftissue temperature reaches 1008C, which can result in cardiac per-foration in thin-walled chambers, and is rarely seen in LV scar-related VT. The volume status needs to be carefully monitoredsince a significant amount of irrigation fluid may be administeredduring mapping and ablation.

Potential complications include stroke, cardiac tamponade, valveinjury, and atrioventricular block. Procedure-related death is seenin 0–3% of the patients, but is most commonly due to

Figure 2 Findings illustrating some of the steps in an ablation procedure for ventricular tachycardia due to prior anterior wall infarction areshown. In (A), programmed ventricular stimulation induces sustained monomorphic ventricular tachycardia. The 12-lead electrocardiographicleads are shown from the top and a recording from the right ventricular apex at the bottom of the panel. Induced ventricular tachycardia has aright bundle branch block—like configuration in V1 and a frontal plane axis directed superiorly, indicating an exit in the inferior wall of the leftventricle. Next, left ventricular access is obtained and a voltage map of the left ventricular created (B). The map is shown as viewed from the leftanterior oblique projection. Purple indicates a normal voltage of .1.5 mV. Blue, green, yellow, and red indicate progressively lower voltages,consistent with the anterior wall infarct scar. A grey region indicates an electrically unexcitable scar, where pacing fails to capture. During cre-ating of the voltage map, pace mapping is performed at low-voltage sites (C). At the site indicated by the arrow, pacing produces a QRS that hasa right bundle branch block configuration and similar, although not identical, axis to the induced ventricular tachycardia, suggesting that theventricular tachycardia exit is in that region of the ventricle. The stimulus to QRS interval of 90 ms is consistent with slow conductionaway from the pacing site. In this case, a decision was made to induce ventricular tachycardia and assess the relation of the region identifiedby pace mapping, to the ventricular tachycardia. (D) Findings during induced ventricular tachycardia. First, note that the ventricular tachycardiathat was induced is different (V1 is isoelectric and the axis is directed more leftward) from the initial ventricular tachycardia shown in (A), pos-sibly indicating a different reentry circuit. However, at this site, electrograms recorded from the mapping catheter electrodes (Abl d, Abl m, andAbl p) have diastolic components and double potentials, suggesting a possible isthmus. Entrainment mapping was performed at this site bypacing slightly faster (cycle length 370 ms) than the ventricular tachycardia (cycle length 385 ms) and the last three stimuli of the pacingtrain are shown. These capture and accelerate the ventricular tachycardia to the pacing rate without changing the QRS morphology, whichis also consistent with pacing from a reentry circuit isthmus. Based on these findings, radiofrequency ablation was performed at this siteduring ventricular tachycardia (E). Ablation terminated ventricular tachycardia, providing further evidence that the site is in the ventriculartachycardia reentry circuit. Additional radiofrequency lesions were then placed in the region to attempt to ensure adequate ablation. Pro-grammed ventricular stimulation was then repeated (data not shown) to determine whether this ventricular tachycardia has been renderednot inducible and determine whether other ventricular tachycardias are inducible, which may warrant further ablation. A purely substrate-basedapproach, ablation during sinus rhythm at all sites with late potentials or where pacing matched the induced ventricular tachycardia morpholo-gies, could also have been considered and would have included the area identified by mapping during ventricular tachycardia.


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uncontrollable VT when the procedure fails.7,8,10 –12 Following suc-cessful ablation, periprocedural death may be the result of sepsisor progressive heart failure. If attempts at endocardial and epicar-dial ablation fail, particularly if the reentry circuit is located deepwithin scar involving the septal myocardium, transcoronaryethanol ablation may be used.46

Procedural endpointsIt is important to note that to date, the best ablative strategy isunknown. No randomized trial has compared ablation during VTwith a substrate-based approach. In addition, no randomized dataare currently available on the best substrate-based approach,that is, comparing isthmus (channel) ablation to a linear lesion ap-proach targeting VT exit sites vs. an encircling technique.

The common absence of a 12-lead ECG of the clinical VT andthe presence of multiple inducible VTs often complicate the as-sessment of the effect of the ablation at the end of the procedureand definition of the ablation endpoint. If mapping is performedduring VT, the minimal procedural endpoint should be non-inducibility of all clinical VTs. Many centres also target all inducibleVTs that are slower than the slowest clinical VT. After ablation ofthe clinical VT, faster VTs may remain inducible with aggressiveprogrammed stimulation.

While non-inducibility has been linked to better outcome,Calkins et al.7 reported no apparent benefit in outcome if all map-pable VTs were rendered non-inducible.8,47 In the VTACH study,successful ablation was defined as non-inducibility of any VT.9 Ina subanalysis of the VTACH study, Wissner et al.48 reported thatacute ablation success did not translate into greater freedom

Figure 3 Bipolar voltage map of the left ventricle (inferior projection). Substrate mapping and ablation during sinus rhythm in a patient withan inferior left ventricular aneurysm secondary to a previous myocardial infarction. Normal voltage (.1.54 mV) is colour-coded in purple, whileabnormal low-amplitude potentials are denoted by colours ranging from blue, green, and yellow to red. Pathological, very low-amplitude (red)potentials are found along the inferior left ventricular wall corresponding to an aneurysm due to previous myocardial infarction. The yellow dotsrepresent potentials recorded from the His–Purkinje conduction system. The blue dots represent areas of late potentials where pace mappingdemonstrated a good (11/12) or perfect (12/12) pace match. Extensive ablation (red dots) was performed within and along the border zone ofthe inferior aneurysm, extending towards the mitral valve. The clinical, haemodynamically unstable ventricular tachycardia was rendered non-inducible following ablation.


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from recurrent VT or ventricular fibrillation. In addition, inducibilityof VT at the time of catheter ablation had no impact on long-termfreedom from ventricular arrhythmias.

If a substrate-based mapping and ablation approach is utilized,acute procedural success can be defined as the absence of all chan-nels inside the area of interest or linear ablation lines at target sitesalong the infarct scar.9

Catheter ablation in patients withischaemic heart disease

Currently available evidence from clinicaltrialsTo date, results of two randomized prospective multicentrestudies have been published in patients with ICM and VT undergo-ing prophylactic catheter ablation to prevent further VT(Table 1).9,10 The SMASH-VT study, published in 2007, assessedthe role of catheter ablation in patients with previous myocardialinfarction and reduced LV ejection fraction (LVEF) undergoingICD implantation for secondary prevention of sudden cardiacdeath.10 Patients presented with haemodynamically unstable ven-tricular arrhythmias, e.g. ventricular fibrillation, haemodynamicallyintolerable VT or syncope, and inducible VT at the time of theelectrophysiology study. To foster recruitment, patients with ap-propriate first-time ICD shock after implantation of an ICD forprimary prevention were eligible. None of the patients receivedClass I or III antiarrhythmic drug therapy. The control arm under-went ICD implantation only. Importantly, catheter ablation wasperformed utilizing a substrate-guided approach. This includedmapping of the ventricular substrate in sinus rhythm without theneed for VT induction. The primary endpoint was survival freefrom VT (appropriate anti-tachycardia pacing or ICD shocktherapy). During an average follow-up period of 22.5+ 5.5months, there was a significant decrease in appropriate ICDtherapy in the ablation group compared with the control arm(12 vs. 33%, P ¼ 0.007). In addition, the number of appropriateshock deliveries was reduced and there was a trend to a reduction

in the number of patients with electrical storm. Catheter ablationhad no significant impact on mortality. Limitations of theSMASH-VT study include the long recruitment period, no standar-dized anti-tachycardia pacing algorithm, and selection of only high-volume, highly experienced ablation centres.

The multicentre VTACH study, published in 2010, assessed therole of VT ablation in patients with prior myocardial infarction,reduced EF ≤50%, and haemodynamically stable VT.9 Onehundred and ten patients were prospectively randomized to ICDimplantation only or VT ablation at the time of ICD implantation.Ablation was guided by a combination of substrate mapping, activa-tion mapping, and pace mapping. The primary endpoint wasdefined as the time to first recurrence of VT or ventricular fibril-lation. The use of antiarrhythmic medication was at the discretionof the treating physician. The median time to first recurrence ofventricular arrhythmias was longer in the ablation group than theICD only group (18.6 vs. 5.9 months). The Kaplan–Meier analysisdemonstrated a significantly better rate of survival free from recur-rent VT in the ablation group (47 vs. 29%, hazard ratio ¼ 0.61, P ¼0.045). There was no difference in mortality between groups.Upon subgroup analysis, patients with an EF of ≤30% derived nobenefit from catheter ablation, while patients with an EF of.30% demonstrated a statistically significant decrease in arrhyth-mia recurrence. Quality-of-life assessment showed no differencebetween groups. Further evidence is needed to assess the exactrole of catheter ablation in the subgroup of patients with an EFof .30%, since these patients derived the greatest benefit fromVT ablation. Although patients with an EF of ≤30% demonstratedno benefit, the results of VTACH need to be corroborated byfuture studies. Until then, catheter ablation of VT should not bewithheld in patients with low LV function. Lastly, the significantlyhigher number of centres participating in VTACH compared withSMASH-VT (16 vs. 3) and the non-standardized approach to abla-tion used in VTACH may explain the higher rate of VT recurrencewhile findings may be more representative of real-world results.

Three non-randomized studies examined the role of catheterablation in patients with previous myocardial infarction and mul-tiple episodes of VT, despite antiarrhythmic drug therapy(Table 1).7,11,12 The recurrence rate of VT in these studies was47, 56, and 49% during a 6-, 8-, and 12-month follow-up period,respectively. While no periprocedural death was reported in theprospective randomized SMASH-VT and VTACH studies, as wellas in the prospective, multicentre Euro-VT-Study, Calkins et al.7

and Stevenson et al. reported a procedure-related mortality of2.7 and 3.0%.9 –12

A meta-analysis of trials comparing catheter ablation for VT inpatients with structural heart disease to control demonstratedthat VT ablation reduced recurrence of ventricular arrhythmiaswithout significant impact on mortality.49

Electrical storm has been defined as three or more separate epi-sodes of VT within a 24 h period and has been associated withincreased mortality in patients with ICDs. In patients presentingwith electrical storm, catheter ablation may serve as the onlyviable treatment option if antiarrhythmic therapy fails. Carbucic-chio et al.8 prospectively assessed the impact of catheter ablationon short- and long-term outcome in 95 patients presenting withelectrical storm. Coronary artery disease was present in 76% of

Figure 4 (Top) Sinus rhythm QRS complex recorded onsurface electrocardiogram lead V1. (Bottom) Local electrogramrecorded from the distal mapping electrode in an area of the ab-normal myocardium demonstrating a fractionated low-amplitudesignal with a late component (arrow).


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Table 1 Prospective studies on catheter ablation of ventricular tachycardia in patients with ischaemic cardiomyopathy

Studies Patients,n

EF (%) Substrate Treatment Type of VT Mapping Acute success, n(%)

FU (ms) Long-termsuccess

Long-termmortality

Prospective randomized multicentre trials

Kuck et al. 20109 107 ICM VT ablation + ICD vs.ICD only

Only stableVT

Mapping during VT/substrate mapping

22.5 (9)

Active 52 34+10 27 (60%) 47% 10%a

Control 55 34+9 29% 7%a

Reddy et al. 200710 128 ICM VT ablation + ICD vs.ICD only

All VT Substrate mapping 22.5 (5.5)

Active 64 31+10 NAb 88% 9%

Control 64 33+9 67% 17%

P ¼ 0.29

Non-randomized prospective multicentre trials

Tanner 2009 63 30+13 ICM VT ablation All VT Mapping during VT/substrate mapping

51 (81%) 12 (3) 51% 9%c

Stevenson et al.200811

231 25d ICM VT ablation All VT Mapping during VT/substrate mapping

113 (49%) 6e 53% 18%f

Calkins et al. 20007 146 31+13 ICM/NICM VT ablation All VT Mapping during VT/substrate mapping

59 (41%) 8+5 46% 25%g

Non-randomized prospective single-centre trialsi

Niwano 2008 58 37+7 ICM/NICM VT ablation All VT Mapping during VT/substrate mapping

43 (74%) 31+22 75% 16%

Carbucicchio et al.20088

95 36+11 ICM/NICM/ARVC

VT ablation Electricalstorm

Mapping during VT/substrate mapping

85 (89%)h 22+13 63 (66%) 16%

ICM, ischaemic cardiomyopathy; NICM, non-ischaemic cardiomyopathy; VT, ventricular tachycardia; ICD, implantable cardioverter-defibrillator; ARVC, arrhythmogenic right ventricular cardiomyopathy; FU, follow-up.aP-value not given.bAblation performed in SR.cAmong 53 patients completing follow-up.dMedian.eSD not given.fAfter 12 months.gOne-year Kaplan–Meier estimate.hAfter one to three procedures.iPatients undergoing successfull ablation; 35+ 5 in patients with failed ablation.

Catheter

ablationof

VT

inIC

Mvs.N

ICM

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. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

. . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . .

Table 2 Studies on catheter ablation of ventricular tachycardia in patients with non-ischaemic cardiomyopathy

Study Patients,n

Substrate EF (%) Endocardialmapping (%)

Epicardialaccess (%)

Acutecomplications (%)

Acutesuccess (%)

Long-termcomplications (%)

Long-termsuccess, n (%)

FU (ms) Mortalityduring FU (%)

Multicentre experience

Dukkipati etal. 201154

10 HCM 57+13 10/10 (100%) 10/10 (100%) None 8/9 (89%)a 1/10 (10%) 7/9 (70%)a,b 37.4+16.9 Not reported

Sacher 200846 149 NICM 39+16 149/149 (100%) Not reported 12/195 (6.2%)c 99/195(51%)c

Not reported 61% after a medianFU of 1 month

40+29 26/149 (17%)

Single-centre experience

Koplan et al.200653

8 Sarcoid 34+15 8/8 RV, 6/8 LV 2/8 (25%) Not reported 2/8 (25%) Not reported 6/8 (75%) withinfirst 6 ms

(6 ms to 7yrs)

1/8 (13%)

Soejima et al.200425

28 DCM 30+11 20/28 (71%) 7/28 (25%) 2/28 (4%),1 epi, 1endo

17/28 (61%) Not reported 17/28 (61%) 11.1+9.3 1/28 (4%)

Hsia et al.200352

19 NICM 34+11 19/19 (100%) None Not reported 14/19 (74%) Not reported 5/19 (26%)d 22+12 4/19 (21%)

DCM, dilated cardiomyopathy; NICM, non-ischaemic cardiomyopathy; HCM, hypertrophic cardiomyopathy; FU, follow-up.aExcluding one patient without attempted ablation.bDefined as no ICD shock during follow-up.cAccording to a total of 195 procedures performed in 149 patients.dDefined as no VT recurrence.

E.Wissner

etal.

1448D

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the patients. Ventricular tachycardia recurred in 34% but only 8%had recurrence of electrical storm during a median follow-up of22+ 13 months. Two recent studies highlighted the importanceof early intervention and the need for a network of collaboratingmedical centres to optimize ablative treatment in patients sufferingfrom electrical storm.50,51

Catheter ablation in patients withnon-ischaemic cardiomyopathyThere are no prospective, randomized studies examining the roleof catheter ablation in patients with NICM or right ventricular car-diomyopathies. Non-randomized studies have demonstrated thefeasibility of catheter ablation in this heterogeneous patient popu-lation25,52–54 (Table 2). The pathophysiological substrate is morevaried than in ICM patients. In NICM, areas of scar containingVT circuits are often located along the base of the LV aroundthe mitral valve annulus.52 In ARVC/D, fibro-fatty replacement ofnormal myocardial tissue involves the perivalvular area aroundthe tricuspid annulus and pulmonic valve annulus as well as theright ventricular free wall and the septum, while the apex is typic-ally spared.55 In both entities, epicardial ablation is more frequentlyrequired compared with patients with ICM,56,57 consistent with thepathological observation that in myocardial infarction, the wave-front of necrosis initiates at the subendocardial layer spreadingoutward, while in patients with ARVC/D, fibro-fatty replacementprogresses from the subepicardial to the endocardial layer.58,59 Ap-plying a substrate-based mapping technique combining pace-mapping and targeting late potentials for ablation appears to beless successful in patients with NICM than in patients with ischae-mic heart disease.60 Overall, the success rate of catheter ablationfor the treatment of NICM is lower than in patients with priormyocardial infarction.25,52,60 This is probably related to the pro-gressive nature of the disease and the prevalence of epicardialand intramural reentry circuits. In patients with ARVC/D undergo-ing catheter ablation, freedom from VT recurrence rangedbetween 77 and 89% during mid-term follow-up.55,57 However,due to the progressive course of ARVC/D, late recurrence isexpected.

Ventricular tachycardiaoriginating from the PurkinjesystemOccasionally, VT originates from reentry or automaticity in a dis-eased Purkinje system. Most commonly, this takes the form ofbundle branch reentry characterized by a wide QRS complextachycardia with a typical bundle branch block pattern. Underlyingconduction abnormalities in the His–Purkinje system are frequent-ly present with interventricular conduction delay or left bundlebranch block and prolongation of the His to ventricle intervalduring sinus rhythm that will typically shorten during bundlebranch reentrant VT.61 Slowed anterograde conduction withinthe left bundle branch allows a fortuitously timed ventricular extra-systole to advance retrograde up the left bundle branch,

anterograde down the right bundle branch, and then through theseptum, completing the reentrant circuit. Catheter ablation ofthe right bundle branch is curative; however, due to significantdisease of the left bundle branch, severely impaired anterogradeatrioventricular conduction is often present.62 Most affectedpatients have significant underlying heart disease and many haveadditional scar-related VTs, such that implantation of an ICD isoften warranted.

Unresolved issues and futureoutlookTherapy to prevent VT is still warranted in patients with ICDs. Al-though ICDs provide effective termination of VT and prevention ofsudden death, episodes of VT reduce quality of life in patients withICDs.5 Recurrent shocks often cause severe psychological impair-ment and post-traumatic stress syndrome. In addition, VT predictsan increased risk of death and heart failure hospitalizations in ICDrecipients.63 According to the current international guidelines,catheter ablation of VT serves as an adjunct to antiarrhythmictherapy in patients experiencing appropriate ICD shocks.16

However, early referral for catheter ablation following ICD inter-vention has the potential to improve patient mortality as well asquality of life.64 In order to evaluate the role of catheter ablationin patients with prior myocardial infarction and recurrent VTdespite antiarrhythmic drug therapy, the VANISH study will ran-domize patients to continued antiarrhythmic drug therapy or cath-eter ablation (ClinicalTrials.gov identifier: NCT00905853). Theprimary endpoint is a composite of mortality and recurrent VT.

Although single-centre series often report favourable outcomesin 70–80% of the patients, in multicentre trials in patients withdrug-refractory, recurrent VT, as discussed above, approximatelyhalf of the patients experience at least one episode of recurrentVT after ablation, although the frequency of VT episodes is sub-stantially improved in the majority. Judging the true effect of cath-eter ablation on patient outcome is often complicated bypost-procedural continuation of antiarrhythmic medication. Fur-thermore, the various mechanisms of VT recurrence followingcatheter ablation are poorly understood. Inadequate lesion forma-tion, deep intramural reentry circuits, or previously dormantreentry circuits might contribute to recurrence.65 It is hopedthat new ablation technologies including intramural needle ablationcatheters may help to overcome some limitations. Advances inimaging technology may aid in the detection of appropriate abla-tion targets. Recently, contrast-enhanced MR imaging has demon-strated a value in delineating conducting channels within scar aspotential targets for ablation.66 Furthermore, intraproceduralcontact-force measurement may improve transmural lesion forma-tion. An epicardial substrate may be more commonly detected inpatients undergoing repeat ablation.26 To date, there is no consen-sus on the appropriate timing of epicardial mapping and ablation.

In patients with VT and relatively good ventricular function(LVEF ≥0.35), ICDs have not been shown to improve mortality.67

In the VTACH study, patients with an EF of .30% and stable VTdemonstrated a significant reduction in recurrent ventricular


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arrhythmias.9 Whether these patients could be safely spared ICDimplantation following successful catheter ablation is not known.

Patients with recurrent VT often have relatively severe heartdisease. Data regarding efficacy and risks of catheter ablation isderived largely from experienced centres. Although we believethat the present data support the earlier use of catheter ablation,prior to multiple symptomatic VT episodes that may result insevere psychological trauma, ablation should continue to be theprevue of experienced centres, appropriately equipped tomanage the occasionally serious complications that can occur.With broader use, continued assessment of outcomes iswarranted.

There is no evidence that catheter ablation of VT reduces mor-tality. A future, sufficiently powered, prospective randomized studyusing standardized ablation and follow-up protocols will need toanswer this important question.

Clinical summaryCatheter ablation methods have improved substantially over thepast two decades. During this time, ICDs have emerged as themajor therapy for protecting patients from sudden death, buthave created a cohort of patients with ventricular arrhythmiasthat reduce quality of life and are associated with increased mor-tality. Antiarrhythmic drug therapy for ventricular arrhythmiashas been disappointing. In view of these considerations, catheterablation, performed in an experienced centre, should be consid-ered early in the management of patients with heart disease whosuffer recurrent symptomatic monomorphic VT. Selection of thistherapy should be made with careful consideration of risks and ef-ficacy, which is importantly influenced by the type and severity ofthe underlying heart disease.

Conflict of interest: none declared.

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