Epicardial Ablationof IdiopathicVentricularTachycardia

Alexander I. Green, MD*, David J. Wilber, MD

KEYWORDS

� Arrhythmia � Ventricular tachycardia� Ablation � Epicardium

om

Idiopathic ventricular tachycardia (VT) describesventricular arrhythmias in the absence of structuralheart disease. Most idiopathic VT originates fromthe right ventricular (RV) outflow tract (OT) in closeproximity to the pulmonic valve. However, idio-pathic VT may arise from other right ventricularsites, including the pulmonary artery1,2 andtricuspid annulus,3 and left ventricular sites,predominately the left ventricular (LV) outflow tract(OT). VT from the aortic sinus cusps (ASC)4 and theepicardium (EPI) remote from the ASCs has beenincreasingly reported. In the authors’ experience,approximately 10% of patients referred for abla-tion of ventricular arrhythmias have an epicardialfocus. As with typical RVOT VT, radiofrequencyablation (RFA) of EPI-VT is a safe and effectivemeans of treating these arrhythmias.

ELECTROPHYSIOLOGICAL CHARACTERISTICS

Idiopathic VT arising from the RVOT and LVOTshares a common mechanism consistent withcyclic adenosine monophosphate (cAMP)-medi-ated triggered activity,5 despite varied clinicalpresentations of sustained VT, bursts of nonsus-tained monomorphic VT, or frequent prematureventricular contractions (PVCs).6 Characteristicfindings of triggered arrhythmias include inabilityto entrain VT, catecholamine enhancement, andtermination with adenosine. In the authors’ initialexperience, they noted catecholaminergic facilita-tion of sustained VT in 11 of 12 patients and

Department of Cardiology, Cardiovascular Institute, LoyoMaywood, IL 60153, USA* Corresponding author.E-mail address: aigreen1075@yahoo.com (A.I. Green).

Card Electrophysiol Clin 2 (2010) 81–91doi:10.1016/j.ccep.2009.11.0061877-9182/10/$ – see front matter ª 2010 Published by E

termination of tachycardia with adenosine in 8 of9 patients. Stellbrink and colleagues7 also reporteda case of EPI-VT terminated with adenosine. Thesefindings support triggered activity as the mecha-nism of EPI-VT. Unique to EPI-VT, however, is theapparent perivascular origin of tachycardia, whichhas been widely reported.8–11 Although atrial fibril-lation is often associated with the musculature ofthe thoracic veins and the ligament of Marshall,the anterior interventricular vein (AIV) and distalgreat cardiac vein (GCV) from which EPI-VTfrequently arises do not have a muscular coat.The proximal coronary sinus, a few millimetersproximal to the GCV, and the proximal middlecardiac vein (MCV) have a muscular coat and arereported, albeit infrequent, sites of origin for EPI-VT.12 The media of the coronary veins do containmyocytes derived from primitive right atrial cells,but their role in the genesis of VT has not beenwell elucidated.13 Further research is needed toclarify the mechanistic relationship between EPI-VT and the coronary veins.

ELECTROCARDIOGRAPHIC ANALYSIS

Analysis of the surface electrocardiogram (ECG)remains the first method of VT localization and isinvaluable in planning an ablation strategy.EPI-VT most often originates from the anteriorsummit of the heart at the AIV, distal GCV, orAIV-GCV junction. As such, a left bundle branch

la University Medical Center, 2160 South First Avenue,

lsevier Inc. card

iacE

P.th

ecli

nics

.c

Green & Wilber82

block (LBBB) inferior axis QRS morphologygrossly similar to RVOT VT is frequently observed.EPI-VT originating from the MCV or proximal coro-nary sinus may have a right bundle branch block(RBBB) or LBBB and superior axis morphology,and it must be distinguished from inferior mitralannular or posterior papillary muscle VT.

Algorithms for localization of VT within theoutflow tracts have relied on several criteria, noneof which reliably identifies EPI-VT. The precordialtransition is defined by the precordial lead in whichthe R/S ratio is greater than or equal to 1. Tannerand colleagues14 described 3 different ablationapproaches for patients in whom the precordialtransition was observed in V3 including ablationfrom the epicardium, RVOT, and LVOT. A late tran-sition greater than or equal to V4 is observed exclu-sively in RVOT VT.15,16 An S wave in leads V5 and V6

is reported to distinguish endocardial LVOT VTfrom foci above the aortic valve.17 However, moreproximal coronary venous foci, including MCVEPI-VT, may inscribe a V6 S wave.7,11 A prominentS wave in lead I may be observed in anteroseptalRVOT VT, ASC-VT, and EPI-VT.14,18–20 Ouyangand colleagues21 proposed the R/S amplitudeindex greater than or equal to 0.3 and the R-waveduration index greater than or equal to 0.5 in leadsV1 or V2 to identify ASC-VT, but these criteria aretypically met for most left ventricular VTs, includingEPI-VT.15 In the authors’ experience, however,some EPI-VT foci in the distal AIV and AIV-GCVjunction may not satisfy either precordial R wavecriteria and may be virtually indistinguishable fromRVOT VT. A Q-wave ratio of leads aVL to aVRgreater than 1.4 and an S-wave amplitude in V1

greater than or equal to 1.2mV may distinguishEPI-VT from ASC-VT when the precordial R-waveindices are met. These criteria are derived in partfrom pace-mapping studies performed from theAIV-GCV junction, and extrapolation to all EPI-VTmay not be justified.19 The authors have seen onepatient with EPI-VT in whom the V1 S wave wasgreater than 1.2mV, but the precordial R-waveindices were not fulfilled. In their patients, no statis-tically significant difference was observed in theQ-wave ratio of aVL to aVR between EPI-VT andASC-VT, although a larger value was observed forASC-VT, contradicting previously reported data(1.13 � 0.34 vs 1.48 � 1.70, P 5 .3).19

In their laboratory, the authors apply the metricof the maximum deflection index (MDI) to identifyEPI-VT.22 It is calculated as follows. The QRSduration is measured as the interval between theearliest rapid deflection of the ventricular complexin any of the simultaneous leads to the latest offsetin any lead. Time to maximum deflection ismeasured from the onset of the QRS complex to

the maximum deflection in each of the precordialleads; the timing of the maximum deflection is atthe largest amplitude deflection above or belowthe isoelectric line. The time to maximum deflec-tion is divided by the QRS duration to obtain theMDI for each precordial lead (Fig. 1). The earliestprecordial maximum deflection (shortest precor-dial MDI) is used to classify the tracing. In theauthors’ initial experience, an MDI of 0.55 orgreater was identified as the optimal cutoff pointfor the detection of EPI-VT remote from theASCs.22 When applied to their current data set of240 cases of idiopathic VT, the earliest precordialMDI remains a reasonable discriminator ofEPI-VT (sensitivity 79.1%, specificity 93.3%).Ventricular arrhythmias arising from the pulmonaryartery (PA) or ASCs represent the greatest numberof false-positives, although occasionally, a pro-longed MDI may be observed in VT of right ventric-ular endocardial origin (Fig. 2).

Additional ECG criteria have been proposed foridentification of EPI-VT in the setting of ischemic ornonischemic cardiomyopathy23,24 but appear tobe less useful in patients with idiopathic VT.

Future directions for the noninvasive localizationof EPI-VT may include electrocardiographicimaging (ECGi). ECGi uses 250 electrodes torecord body-surface potentials in conjunctionwith a heart-torso computed tomography registra-tion to construct epicardial activation and repolar-ization and to permit construction of virtualepicardial electrograms. An exclusively negativeQS complex without an initial R wave in virtualelectrograms at the site of origin may signify anepicardial focus. However, experience with ECGiimaging for idiopathic VT is limited,25,26 and furtherexperience will be required to validate thisconcept.

CATHETER ABLATION

Patients with a prolonged MDI on the surface ECGand those in whom prior comprehensive endocar-dial mapping and ablation were unsuccessful arethe most likely to have an epicardial origin of VT.In these patients, the authors find it useful to placea 3.5F, 16-pole microwire with 2-6-2–mm spacing(Pathfinder; Cardima Inc, Fremont, CA, USA)through the coronary sinus and position it tospan the distal GCV, AIV-GCV junction, and distalAIV at the start of the study (Fig. 3B). This regionrepresents the most common origin of idiopathicepicardial VT with an inferior axis. For patientswith a high probability of an epicardial originwhose limb-lead axis is superior, the microwire isbest positioned in the middle cardiac vein. Anelectrogram to QRS onset in the microwire of

Fig. 1. Calculation of the MDI. The earliest time to maximum deflection (TMD) in any of the precordial leads (inthis example, lead V3) is measured and divided by total QRS duration (QRSd). (Reprinted with permission).

Epicardial Ablation of Idiopathic VT 83

approximately 35 to 40 milliseconds pre-QRSsuggests an epicardial focus and permits a morefocused and efficient approach to mapping.However, to confirm the epicardium as the earliestactivation site before ablation, the coronary

Ep ica rdia l

Fasc icu la r

LVOT

Pu lm A

Loc

0.1

0.2

0.3

0.4

0.5

0.6

0.7

0.8

MD

I

Fig. 2. The distribution of values for MDI for the differenMDI of 0.55.

venous activation must still be carefully comparedwith activation in the ASC, RV, PA, and LV endo-cardium for inferior axis VTs and with the RV andLV endocardium for superior axis VTs. When thesuspicion of an epicardial origin is high and the

rtery

Pap illary

RVOTASC

ationt anatomic locations. The dashed line demarcates an

Fig. 3. (A) The ECG of an AIV-GCV tachycardia. (B) The RAO and LAO projections of the 16-pole microwire span-ning the AIV-GCV junction (top row) and successful ablation site in relation to the coronary arteries (bottom row).(C) The timing of the earliest electrogram to QRS onset (41 milliseconds) in the microwire suggesting an epicardialorigin. (D) Spontaneous VT to pace-mapping match of 97% at the successful ablation site with the use of auto-mated software (PASSO, Diamond Bar, CA, USA). RAO, right anterior oblique; LAO, left anterior oblique.

Green & Wilber84

Fig. 3. (continued)

Epicardial Ablation of Idiopathic VT 85

86

Epicardial Ablation of Idiopathic VT 87

authors anticipate a subxyphoid approach, this isgenerally performed before the administration ofheparin and mapping of the left ventricle and aorticroot. Once epicardial access is obtained, thepatient may be given heparin to achieve an acti-vated clotting time of 250 milliseconds or greater.

An epicardial origin is confirmed via a combina-tion of multichamber electroanatomic mappingand pace mapping, the latter being particularlyvaluable when there is little spontaneous ventric-ular ectopy. However, caution should be exercisedin proceeding with epicardial ablation based onpace mapping alone in the absence of confirma-tory activation mapping. Pace mapping has, atbest, modest spatial resolution, and pacing overa fairly large area (up to 2–3 cm2) may produceexcellent pace-map matches.27,28 These studiesaddress pace mapping as a means of localizingRVOT-VT and may not apply directly to EPI-VT.The authors have occasionally observed excellentpace-map matches from the epicardium or ASC insites successfully ablated from the endocardium,and vice versa, pace mapping from the epicardiumand ASCs frequently requires pacing at highoutputs that may influence the QRS morphology.Finally, the absence of noninducibility or abolitionof spontaneous arrhythmias as a proceduralendpoint is suboptimal. It is therefore the authors’practice to make vigorous attempts to reproducethe clinical arrhythmia (stimulation from multiplesites and use of intravenous isoproterenol,epinephrine, or phenylephrine) for activationmapping, and to use pace mapping predominantlyas a corroborative measure. Phenylephrine isparticularly useful for long-coupled PVCs andbradycardia-dependent arrhythmias.

Catheter ablation of EPI-VT may be attemptedvia 2 different approaches. The first approach isto map the coronary sinus and its tributaries. Giventhe perivenous origin of most idiopathic EPI-VT,ablation from within the veins may be successful,although maximum delivery of power with 4-mmelectrodes may not exceed 15 to 20 W. The useof irrigated tip catheters to improve power deliveryin the coronary sinus may be reasonable before

Fig. 4. (A, B) Surface ECG and intracardiac electrograms fro(A) The left half of the panel demonstrates the 12-lead Ecycle length. Pacing from the ablation site (right half ofin all 12 leads. (B) Recordings from the distal bipole of ththe venous epicardial mapping catheter in the GCV. Activ(C) Termination of VT in 2 seconds after onset of radiofreof 60�C. (D) Occlusive venogram demonstrating the coronvein with a takeoff from the proximal GCV (small arrowheMultipolar microcatheters in the GCV (large arrowheads)strated. (F) 6F 4-mm electrode catheter positioned in theof successful VT ablation (small arrowhead).

:

a subxiphoid approach. It has been recommendedby some investigators that a maximum of 20 W beused in the coronary veins to limit the risk of coro-nary injury or hemopericardium.9 The tortuosity,angulation, and small caliber of the coronary veinsoften limits successful navigation to the site oforigin. The distal GCV and AIV-GCV junction runparallel with the proximal circumflex coronaryartery and the distal AIV, with the left anterior de-scending artery. For this reason, angiographyshould be performed before and following abla-tion. Figs. 3 and 4 demonstrate examples of trans-venous ablation of EPI-VT from theAIV-GCV junction and more proximal GCV.

When venous mapping and ablation are unableto eliminate VT, direct pericardial access is accom-plished by a subxiphoid approach as described bySosa and colleagues.29 Patients with EPI-VT andstructurally normal hearts in whom prior sternoto-my has been performed may require a combinedapproach of surgical subxiphoid epicardial expo-sure. Even then, dense adhesion may limit accessto the anterior, superior epicardial surface.30 Abla-tion in the pericardial space carries important limi-tations in the delivery of adequate power ascompared with the endocardial surface. Specifi-cally, the lack of convective cooling of the ablationelectrode by the blood and the relatively thick layerof adipose tissue that often overlays the perivenousVT foci may hamper ablation attempts. In animalmodels, d’Avila and colleagues31 demonstratedthat standard RFA produced significant lesions(3.7 � 1.2 mm thick) on epicardial tissue withoutan interposing adipose layer, but they were unableto produce myocardial lesions when applied tonormal tissue with epicardial fat (3.1 � 1.2 mmthick). However, the use of cooled-tip RFA ina closed chest animal model resulted in appre-ciable myocardial lesions (4.07 � 2 mm depth)when applied to tissue with overlying fat (2.6 �1.2 mm thick). The volume of epicardial fat hasbeen correlated to visceral adiposity, increasedbody mass index, female gender, and increasedage. Cardiovascular magnetic resonance imagingand multi-detector computed tomography to

m a patient with VT from the distal great cardiac vein.CG during tachycardia. Note the slight irregularity ofpanel) results in an exact match of QRS morphologye ablation catheter (arrowhead) and bipolar pairs ofation at this site is 53 milliseconds before QRS onset.quency energy application of 5 W and a temperatureary sinus and proximal GCV. There is a small marginalad). (E) RAO radiographs of coronary venous mapping.and marginal branch (small arrowheads) are demon-proximal portion of the marginal branch at the site

Table 1Location of ablation sites for idiopathicepicardial VT (N530)

I. Epicardial sites adjacent to the coronaryvasculature

a. Proximal AIV 6

b. AIV-GCV junction 9

c. GCV 4

d. MCV 3

II. Intramural sites

a. Anterobasal left ventricle 5

b. Base of the papillary muscle 2

III. Other

Tricuspid annular 1

Green & Wilber88

quantify the distribution and thickness of epicardialadipose tissue may prove beneficial in planningepicardial procedures.32,33

Thermal injury to adjacent coronary vessels withthe potential for acute thrombosis or futurestenosis is important to consider during ablation.In addition to applied power, the main factors pre-dicting coronary injury are the distance from theablation catheter to the arterial wall and the sizeof the arterial vessel. It has been empirically rec-ommended that ablation within 5 to 10 mm ofa coronary vessel be avoided. Animal studieshave demonstrated that standard RFA withinapproximately 0.3 mm of the arterial wall has thepotential to cause intravascular thrombosis orsignificant intimal hyperplasia, whereas RFA deliv-ered from distances greater than 0.3 mm maycause replacement of the arterial media with extra-cellular matrix.34 The long-term consequences ofthe latter are unknown, and extrapolation topatients should be made with caution. Addition-ally, these studies were not performed with irri-gated tip catheters where greater lesion size maybe achieved. It is the authors’ practice to performcoronary angiography before ablation to assessthe proximity of the coronary arteries. Ablation isthen performed with initially low power and titra-tion of power, with careful attention paid to hemo-dynamic stability and the ST segments for anyevidence of acute elevation or depression sugges-tive of myocardial injury. A repeat angiogram isperformed within 30 minutes following ablation.The overall risk of coronary injury is estimated atless than 1%. Intracoronary irrigation with chilledsaline has been proposed as a mechanism forreducing the risk of heat-related coronary injury,although this maneuver has not been widely adop-ted in clinical practice.35

Ablation within the epicardial space can alsocause phrenic nerve injury, and high output pacingto identify phrenic capture is advisable to avoid thiscomplication. A recent cadaveric study demon-strated that the phrenic nerve may run in an anteriorcourse parallel to the anterior interventricular within4 mm of the left main coronary artery.36,37 This high-lights the proximity of the AIV-GCV junction to thepericardiophrenic neurovascular bundle. Severalstrategies, including the infusion of saline or airinto the pericardial space or the use of large-diam-eter balloons to ‘‘lift’’ the nerve from the epicardialsurface, have been proposed to avoid phrenicnerve injury. The introduction of a combination ofair and saline to create an iatrogenic ‘‘hydropneu-mopericardium’’ has also been proposed.36

In the authors’ experience, an epicardialapproach is useful in 3 different clinical scenarios(Table 1). The first was in 21 patients (mean age

39 years, range 11–74 years) with 22 tachycardiasthat were perivenous in origin typical of thosepreviously reported. In this population, the earliestepicardial local activation times (42 � 5 millisec-onds) significantly preceded endocardial activa-tion times (22 � 5 milliseconds). In patients inwhom VT was localized to the AIV or AIV-GCVjunction, local activation times in the ASCs weresignificantly later than those recorded from theepicardium (13 � 18 milliseconds). Ablation wassuccessful in the elimination of 17 of 22 ventriculararrhythmias via a coronary venous approach in 8cases, percutaneous epicardial approach in 7,and open surgical approach in 2. In 5 patients,the elimination of VT was ultimately unsuccessful.One patient refused a percutaneous epicardialapproach following failed ablation via a coronaryvenous approach. In one patient, the left maincoronary artery and AIV-GCV junction were tooclosely approximated to allow safe RFA. Phrenicnerve capture limited ablation in one patient. Theauthors were unable to access the pericardialspace in one patient; however, the PVC burdenon subsequent ambulatory monitoring was lessthan 1% off all antiarrhythmic medications despiteectopy at the end of the procedure. The lastpatient had persistent ectopy following transperi-cardial ablation despite the use of an irrigated tipcatheter and cryoablation.

The second scenario in which epicardial abla-tion has a role is in patients with an apparent intra-mural ectopic focus. These sites were usually notintimately associated with the coronary vascula-ture. The authors performed ablation of 7 VTmorphologies in 7 patients (mean age 29 years,range 14–53 years). The distribution of VT wasthe anterior base of the left ventricle in 5 patientsand the base of the papillary muscle in 2 patients

Fig. 5. Radiographs (A) and (B) demonstrate the epicardial catheter position in relation to the coronary arteriesbefore ablation in a patient with intramural VT localized to the base of the anterolateral papillary muscle. (C) Theintracardiac echocardiogram demonstrated the ablation catheter tip (large, white arrow) at the base of the papil-lary muscle.

Epicardial Ablation of Idiopathic VT 89

(Fig. 5). The earliest local activation times from theepicardial and endocardium were nearly equal andwithin 10 milliseconds of each other (38 � 4 milli-seconds EPI vs 35� 7 milliseconds endocardium).In each case, ablation at the site with the earliesttime (either epicardial or endocardial) was notsuccessful. The authors’ ablation approach wasto ‘‘sandwich’’ the putative VT focus viaa combined endocardial and epicardial approach.Ablation was successful in 3 of 5 patients ablatedat anterobasal LV sites and both patients with

papillary muscle VT. The latter 2 patients werepart of 10 patients with idiopathic papillary muscleVT undergoing ablation at the authors’ institution.Prior reports on idiopathic papillary muscle VThave not described this approach.36

In a final patient, VT originated from the superiorlateral aspect of the right ventricle, adjacent to thetricuspid annulus. This VT was reentrant as deter-mined by entrainment and originated from a smallregion of epicardial low voltage. The patient hadundergone an extensive and repeated workup for

Green & Wilber90

arrhythmogenic right ventricular cardiomyopathyand has developed no other task force criteriaduring 5 years of follow-up.

As previously mentioned, the authors routinelyperform preablation angiography to demonstratethe proximity of the coronary arteries to theplanned site of ablation and perform high-outputpacing to document the presence of absence ofphrenic nerve capture. During ablation, they limittheir power settings to 20 to 30 W in the coronaryveins, but up to 50 W may be required on theepicardial surface at sites remote from epicardialvasculature. During coronary venous ablation,standard RFA catheters are often unable to effec-tively deliver power, necessitating the use of anirrigated tip catheter. When ablating from theepicardium via a subxyphoid approach, theauthors typically use irrigated tip catheter ablationfrom the outset.

SUMMARY

Epicardial VT is an increasingly recognizedarrhythmia in clinical practice. ECG algorithms toidentify epicardial VT should be used with theunderstanding that they are an initial guide tolocalization and do not exclude an epicardial originof VT, particularly when endocardial approachesare unsuccessful. Ablation using a transvenousapproach or direct epicardial access may producefavorable results, although care must be takento avoid coronary artery or phrenic nerve injury.A subset of patients require a combined endocar-dial and epicardial approach to eliminate VT.Although these ablation strategies are generallywell tolerated, they should be limited to patientswith highly symptomatic arrhythmias or those inwhom myocardial depression is thought to berelated to prolonged tachycardia or repetitiveventricular ectopy.

REFERENCES

1. Sekiguchi Y, Aonuma K, Takahashi A, et al. Electro-

cardiographic and electrophysiologic characteris-

tics of ventricular tachycardia originating within the

pulmonary artery. J Am Coll Cardiol 2005;45(6):

887–95.

2. Tada H, Tadokoro K, Miyaji K, et al. Idiopathic

ventricular arrhythmias arising from the pulmonary

artery: prevalence, characteristics, and topography

of the arrhythmia origin. Heart Rhythm 2008;5(3):

419–26.

3. Tada H, Tadokoro K, Ito S, et al. Idiopathic ventricular

arrhythmias originating from the tricuspid annulus:

prevalence, electrocardiographic characteristics,

and results of radiofrequency catheter ablation. Heart

Rhythm 2007;4(1):7–16.

4. Kanagaratnam L, Tomassoni G, Schweikert R, et al.

Ventricular tachycardias arising from the aortic sinus

of valsalva: an under-recognized variant of left

outflow tract ventricular tachycardia. J Am Coll

Cardiol 2001;37(5):1408–14.

5. Iwai S, Cantillon DJ, Kim RJ, et al. Right and left

ventricular outflow tract tachycardias: evidence for

a common electrophysiologic mechanism. J Cardio-

vasc Electrophysiol 2006;17(10):1052–8.

6. Kim RJ, Iwai S, Markowitz SM, et al. Clinical and

electrophysiological spectrum of idiopathic ventric-

ular outflow tract arrhythmias. J Am Coll Cardiol

2007;49(20):2035–43.

7. Stellbrink C, Diem B, Schauerte P, et al. Transcoro-

nary venous radiofrequency catheter ablation of

ventricular tachycardia. J Cardiovasc Electrophysiol

1997;8(8):916–21.

8. Meininger GR, Berger RD. Idiopathic ventricular

tachycardia originating in the great cardiac vein.

Heart Rhythm 2006;3(4):464–6.

9. Obel OA, d’Avila A, Neuzil P, et al. Ablation of left

ventricular epicardial outflow tract tachycardia from

the distal great cardiac vein. J Am Coll Cardiol

2006;48(9):1813–7.

10. Wright M, Hocini M, Ho SY, et al. Epicardial abla-

tion of left ventricular outflow tract tachycardia via

the coronary sinus. Heart Rhythm 2009;6(2):

290–1.

11. Doppalapudi H, Yamada T, Ramaswamy K, et al.

Idiopathic focal epicardial ventricular tachycardia

originating from the crux of the heart. Heart Rhythm

2009;6(1):44–50.

12. von Ludinghausen M. The venous drainage of the

human myocardium. Adv Anat Embryol Cell Biol

2003;168:1–104.

13. Vrancken Peeters MP, Gittenberger-de Groot AC,

Mentink MM, et al. Differences in development of

coronary arteries and veins. Cardiovasc Res 1997;

36(1):101–10.

14. Tanner H, Hindricks G, Schirdewahn P, et al.

Outflow tract tachycardia with R/S transition in

lead V3: Six different anatomic approaches for

successful ablation. J Am Coll Cardiol 2005;

45(3):418–23.

15. Ito S, Tada H, Naito S, et al. Development and vali-

dation of an ECG algorithm for identifying the

optimal ablation site for idiopathic ventricular outflow

tract tachycardia. J Cardiovasc Electrophysiol 2003;

14(12):1280–6.

16. Tanner H, Wolber T, Schwick N, et al. Electrocardio-

graphic pattern as a guide for management and

radiofrequency ablation of idiopathic ventricular

tachycardia. Cardiology 2005;103(1):30–6.

17. Hachiya H, Aonuma K, Yamauchi Y, et al. How to

diagnose, locate, and ablate coronary cusp

Epicardial Ablation of Idiopathic VT 91

ventricular tachycardia. J Cardiovasc Electrophysiol

2002;13(6):551–6.

18. Wilber DJ, Baerman J, Olshansky B, et al. Adeno-

sine-sensitive ventricular tachycardia. clinical char-

acteristics and response to catheter ablation.

Circulation 1993;87(1):126–34.

19. Tada H, Nogami A, Naito S, et al. Left ventricular

epicardial outflow tract tachycardia: A new distinct

subgroup of outflow tract tachycardia. Jpn Circ J

2001;65(8):723–30.

20. Kaseno K, Tada H, Tanaka S, et al. Successful catheter

ablation of left ventricular epicardial tachycardia orig-

inating from the great cardiac vein: a case report and

review of the literature. Circ J 2007;71(12):1983–8.

21. Ouyang F, Fotuhi P, Ho SY, et al. Repetitive mono-

morphic ventricular tachycardia originating from

the aortic sinus cusp: electrocardiographic charac-

terization for guiding catheter ablation. J Am Coll

Cardiol 2002;39(3):500–8.

22. Daniels DV, Lu YY, Morton JB, et al. Idiopathic

epicardial left ventricular tachycardia originating

remote from the sinus of valsalva: electrophysiolog-

ical characteristics, catheter ablation, and identifica-

tion from the 12-lead electrocardiogram. Circulation

2006;113(13):1659–66.

23. Bazan V, Gerstenfeld EP, Garcia FC, et al. Site-

specific twelve-lead ECG features to identify an

epicardial origin for left ventricular tachycardia in

the absence of myocardial infarction. Heart Rhythm

2007;4(11):1403–10.

24. Berruezo A, Mont L, Nava S, et al. Electrocardio-

graphic recognition of the epicardial origin of ventric-

ular tachycardias. Circulation 2004;109(15):1842–7.

25. Intini A, Goldstein RN, Jia P, et al. Electrocardio-

graphic imaging (ECGI), a novel diagnostic modality

used for mapping of focal left ventricular tachycardia

in a young athlete. Heart Rhythm 2005;2(11):1250–2.

26. Green A, Brysiewicz N, Finn C, et al. Preliminary

experience with noninvasive electrocardiographic

imaging in patients with idiopathic ventricular tachy-

cardia [abstract]. Circulation 2008;118:S985.

27. Azegami K, Wilber DJ, Arruda M, et al. Spatial reso-

lution of pacemapping and activation mapping in

patients with idiopathic right ventricular outflow tract

tachycardia. J Cardiovasc Electrophysiol 2005;

16(8):823–9.

28. Bogun F, Taj M, Ting M, et al. Spatial resolution of

pace mapping of idiopathic ventricular tachycardia/

ectopy originating in the right ventricular outflow tract.

Heart Rhythm 2008;5(3):339–44.

29. Sosa E, Scanavacca M, d’Avila A, et al. A new tech-

nique to perform epicardial mapping in the electro-

physiology laboratory. J Cardiovasc Electrophysiol

1996;7(6):531–6.

30. Soejima K, Couper G, Cooper JM, et al. Subxiphoid

surgical approach for epicardial catheter-based

mapping and ablation in patients with prior cardiac

surgery or difficult pericardial access. Circulation

2004;110(10):1197–201.

31. d’Avila A, Houghtaling C, Gutierrez P, et al. Catheter

ablation of ventricular epicardial tissue: A compar-

ison of standard and cooled-tip radiofrequency

energy. Circulation 2004;109(19):2363–9.

32. Abbara S, Desai JC, Cury RC, et al. Mapping epicar-

dial fat with multi-detector computed tomography to

facilitate percutaneous transepicardial arrhythmia

ablation. Eur J Radiol 2006;57(3):417–22.

33. Sarin S, Wenger C, Marwaha A, et al. Clinical signif-

icance of epicardial fat measured using cardiac

multislice computed tomography. Am J Cardiol

2008;102(6):767–71.

34. D’Avila A, Gutierrez P, Scanavacca M, et al. Effects

of radiofrequency pulses delivered in the vicinity of

the coronary arteries: Implications for nonsurgical

transthoracic epicardial catheter ablation to treat

ventricular tachycardia. Pacing Clin Electrophysiol

2002;25(10):1488–95.

35. Thyer IA, Kovoor P, Barry MA, et al. Protection of the

coronary arteries during epicardial radiofrequency

ablation with intracoronary chilled saline irrigation:

assessment in an in vitro model. J Cardiovasc Elec-

trophysiol 2006;17(5):544–9.

36. Di Biase L, Burkhardt JD, Pelargonio G, et al.

Prevention of phrenic nerve injury during epicardial

ablation: comparison of methods for separating the

phrenic nerve from the epicardial surface. Heart

Rhythm 2009;6(7):957–61.

37. Good E, Desjardins B, Oral H, et al. Ventricular

arrhythmias originating from a papillary muscle in

patients without prior infarction: a comparison

with fascicular arrhythmias. Heart Rhythm 2008;5:

1530–7.