Sustained Monomorphic VT in Chagas Disease - UCSF CME Hsia Handouts.pdf · p=0.006 VT...

8/29/2016

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VT Ablation 2016: Indications and Expected Outcomes

Henry H. Hsia, MD, FACC, FHRS San Francisco VA Medical Center,

University of California, San Francisco

California Heart Rhythm Symposium

2016

Medtronic: advisory board, review panel

St Jude Medical: speakers bureau

Biosense-Webster: speakers bureau, fellowship support

VytronUs: consultant

Disclosures

Trends in Catheter VT Ablation

N =81,539

Post-infarction VT

UCLA: 6/2004-7/2011

VT in Nonischemic Cardiomyopathy

Sacher F. Circ Arrhythm Electrophysiol 2008;1;153

Nakahara S. JACC 2010;55:2355–2365

Palaniswamy C. Heart Rhythm 2014;11:2056

VT ablation:

The proportion of NICM has

increased from 27% (1999-2002) to

35% (2003-2006) (P=0.06)

Post-infarct VT:

catheter ablation increased

from 2.8% (2002) 10.8%

(2011); (p <0.001).

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Anatomical Substrate Post-Myocardial

Infarction

deBakker J. Circulation 1988; 77:589 deBakker J. Circulation 1993;88;915

Slow conduction in the infarcted tissue,

with ‘zigzag' course of activation

Tung R. Circulation 2011;123:2284

RBRS VT: Entrainment with Concealed Fusion Isthmus, #196

Sti-QRS=Egm-QRS 142 msec

I

II

III

AVR

AVL

AVF

V1

V2

V3

V4

V5

V6

Hisd

RV

Hisp

Abld

Ablp

PPI=360 ms

sti-QRS

142 ms

VTCL=363 ms

Egm-QRS

142ms

Ent

Isth

Exit

RBRS VT

Inferolateral Scar

AoV

Outer

Loop LP 180ms 255

198 190

170

Dysynchrony

on ICE

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Ablation at Isthmus: RBRS VT Termination in 1.5 sec

I

II

III

AVR

AVL

AVF

V1

V2

V3

V4

V5

V6

Hisd

RV

Hisp

Abld

Ablp

Stim

0.5-1.6 mV 0.36-0.55 mV 0.21-0.31 mV

I

II

III

AVR

AVL

AVF

V1

Abld

V2

V3

V4

V5

V6

Ablp

His

RVA

Late potentials with

decremental local

conduction delay

0.21-0.31 mV

LP 171 ms

LP 194 ms

Decremental

LP delay

0.5-1.6 mV

I

II

III

aVR

aVL

aVF

V1

V2

V3

V4

V5

V6

Perfect

pacemap

Spontaneous

LBB-RI VT

Pacemap

within the

channel

LP 180 ms

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P=0.007

Ablation

Control

P=0.045

Kaplan–Meier Estimate of Survival Free from

ICD (Shock & ATP) Therapy Kaplan-Meier Estimates for Survival

Free from VT or VF

SMASH VT Trial VTACH Trial

Thermocool VT

Ablation Trial

N=231, VT (median, 11 in preceding 6 mo), primary

end point of freedom from VT after 6 month f/u.

VT episodes were reduced from a median of 11.5 to

0 (P<0.0001).

Stevenson WG. Circ 2008;118:2773-82

Kuck KH. Lancet 2010; 375: 31–40

Reddy VY. NEJM 2007;357:2657-65.

Ablation

Control

Catheter Ablation in Post-infarct VT

N Indications LVEF

(%)

Acute

success

Follow-up

(months)

Recurrent

VT/ICD Rx

Adverse

events

SMASH-VT

(2007) 64

Recur/induc

VT/VF 31±10 ----- 24 13%* 4.6%

ThermoCool

(2008) 231 MMVT 25 49% 6 47% 7.3%

VTACH

(2010) 52 Stable VT 34±9.6 ----- 21.9±8.3 53% 3.8%

Euro-VT

(2010) 63 Recur VT 30±13 81% 12±3 49% 5%

Yokokawa

(2012) 98

Recur VT

ICD Rx 27±13 63% 35±23 34% 7.1%

Silberbauer

(2014) 155

Drug

refractory VT 31±9.4 ----- ~19 32% 7%

Dinov

(2014) 164 Recur VT 32±11 77.4% 27 43% 11.1%

VT Recurrences After the Ablation Procedure

Thermocool VT Ablation (2008)

Success

(123)

Failure

(108) p

Age 65

(58-70)

69

(62-73) 0.012

Heart failure 52% 73% 0.002

LVEF (%) 25

(20-35)

25

(15-35) 0.387

Multiple MI 5% 14% 0.016

VT events in

prec 6 mo

10

(4-30)

14

(6-38) 0.37

# induced

VT/pt

3

(2-4)

4

(3-6) 0.002

Longest VT

CL

440

(370-500)

450

(380-538) 0.251

Shortest VT

CL

330

(271-400)

305

(272-350) 0.029

Total # RF

lesions

24

(11-32)

26

(16-39) 0.029

Postop VT

Induction 30 58 <0.001

Yokokawa et al (2012)

No recurr

VT (65)

Recurrent

VT (33) p

LVEF (%) 29 ± 14 25 ± 12 0.26

Anterior MI 18 (28%) 14 (42%) 0.14

Scar area

(cm3) 69 ± 30 93 ± 40 0.002

# clinical VT 4 ± 5 3 ± 3 0.29

Clinical VT

CL 359 ± 73 350 ± 77 0.34

# induced

VT 13 (20%) 9 (27%) 0.41

Identified

critical sites 3 ± 2 4 ± 3 0.49

RF duration

(min) 63 ± 44 73 ± 48 0.35

Postop VT-

nonclinical 24/63 (38%) 11/32 (34%) 0.72

Postop VT-

clinical 0/63 (0%) 0/63 (0%) 1.0

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VT Recurrence Rate vs Ablation Strategies

Recurrence Rate During Follow-up 13.4 ± 4 months

0

10

20

30

40

50

60

70

80

90

100All Patients (n=50)

9.5% 12.5%

75%

50%

Complete LP abolition

Incomplete LP abolition

Persistent VT inducibility

No VT inducible

Pe

rce

nta

ge

of

Pa

tie

nts

(%

)

Silberbauer J et al. Circ Arrhythm Electrophysiol, 2014. 7(3):424-435

Freedom from Recurrent VT or Death

Jais P. Circulation 2012;125:2184

Local Abnormal Ventricular Activities

(LAVA)

1 2 3 4

5

Komatsu Y. Heart Rhythm 2013;10:1630

Regional Variation of LAVA Latency

Latency of LAVA is affected by locations. Only 3%

of septal LAVA were separated from far-field

ventricular egm

*

Ventricular Arrhythmia/ICD Therapy-Free Survival by the Ablation Approach

In Post-infarct VT

p=0.006

VT non-inducible+LP abolition

VT non-inducible, no LP abolition

VT inducible

N=92, f/u of 25±10 months

Homogenization (Endo ± Epi): 19%

Endo substrate ablation: 47%

P<0.001

N= 160, f/u ~19 months

Silberbauer J. Circ Arrhythm Electrophysiol. 2014;7:424 DiBiase L . JACC 2012;60:132

16%

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Scar De-channeling

Berruezo A. Circ Arrhythm Electrophysiol. 2015;8:326-336

16.4%

Recurrence after Catheter Ablation of Post-infarct VT

Santangeli et al, Indication for Ablation and Trials, Ventricular Tachycardia Ablation: A Practical Guide, 2014. CardioText

38% RRR

Limited

substrate ablation

Extensive

substrate modification

Differences Between NICM and ICM Substrates

Nakahara S. JACC 2010;55:2355–2365

55±41 53±28

101±55

56±33

Endo Scar and Endo DS area : ICM >> NICM

Endo and Epi LP: ICM >>NICM.

LP-targeted ablation was more effective in ICM (82% non-recurrence at 12±10

mon f/u) vs NICM patients with less favorable outcomes (50% at 15±13 mon f/u).

4.1%

4.3%

1.3% 2.1%

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Epicardial VT Ablation: A Multicenter Safety Study

Characteristics of the Patient Population

Ischemic

CMP

(n=51)

Dilated

CMP

(n=39)

ARVC

(n=14)

No CMP

(n=17)

Other

CMP

(n=13)

Total

patients

(n=134)

Relative to a

control

population(n=722) 16% 35% 41% 6% 18% 19%

Sex (Male %) 48

(94%)

32

(82%)

9

(64%)

10

(59%)

10

(77%)

109

(81%)

Prior endocardial

ablation

46

(90%)

33

(85%)

9

(64%)

15

(88%)

12

(92%)

115

(86%)

Epicardial mapping

and ablation

42

(82%)

36

(92%)

14

(100%)

12

(71%)

9

(69%)

113

(84%)

Sacher F. JACC 2010; 55: 2366

Endo

Epi

Cano O. JACC 2009;54:799–808

Soejima K. JACC 2004; 43;10:1834

Scar area (cm2)

Wide/split/late egm:

epicardial (49.7%)

controls (2.3%).

Epicardial vs Endocardial Low

Voltage Scar Distributions

in Non-Ischemic

Cardiomyopathy

LV endocardium:

minimal scar

LV epicardium:

extensive scar

Endo-Epicardial Mapping in Patient with Nonischemic Cardiomyopathy

I

II

III

AVR

AVL

AVF

V1

V2

V3

V4

V5

V6

RV

Abld

Ablp

Entrainment with

concealed fusion:

Isthmus

MV MV

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Scar Patterns and Ablation in Nonischemic Cardiomyopathy

Basal anteroseptal scar (42%): -aortic root ± anteroseptal endo LV (89%) -anterior cardiac vein (11%), with -RV septum (22%) -epicardium (11%)

Green: good pacemap Yellow: ECF White: VT termination

Inferolateral scar (47%): -epicardium (63%) -inferolateral endo LV (37%)

Piers, S. Circ Arrhythm Electrophysiol. 2013;6:875

INFEROLATERAL GROUP

Nonischemic Cardiomyopathy: Anteroseptal vs Inferolateral Scar

Oloriz, T. Circ Arrhythm Electrophysiol. 2014;7:414-423

Endocardial unipolar voltage: -Anteroseptal (AS): 44/87 (51%) -Inferolateral (IL): 43/87 (49%)

-AS has more extensive endo unipolar scar, freq involves an intramural septal substrate.

Epi LPs: common in the IL (81%) vs AS (4%), p<0.001) and correlated with VT termination sites (p=0.014).

VT recurred in 44 patients (51%) during a median f/u 1.5 years.

AS scar was associated with higher VT recurrence (74% vs 25%, p<0.001) and redo procedure rates (59% vs 7%, p<0.001).

Outcome of Catheter Ablation in Nonischemic Cardiomyopathy

N F/U

(months) Approach

Acute

Noninducibility No Recurrence

Marchlinski

(2000) 8 10 Endo 1 (12%) 3 (38%)

Hsia

(2003) 19 22 Endo 8 (42%) 5 (26%)

Soejima

(2004) 22 11±9

Endo (22)

± Epi (7)

12/22 (55%)

6/6 (100%)

12/22 (55%)

4/6 (67%)

Cano

(2009) 22 18±7 Endo+Epi (22)

14/21 (67%)

12/17 (71%)

15/21 (71%)

12/14 (86%)

Kuhne

(2010) 24 18

Endo (24)

± Epi (7) 45/67 (67%)

67% if LP+

7% if LP-

Della Bella

(2011) 67 17±18

Endo+Epi (57)

Epi only (10) 45/67 (67%) 60.7%

Tung

(2013) 56 12

Endo only (35)

Endo+Epi (29)

40%

45%

33%

36%

Dinov

(2014) 63 20

Endo only (43)

Endo+Epi (20) 42 (66.7%) 23%

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ICM

40.5% 43%

23%

57%

NICM

Outcomes in VT Ablation in Nonischemic vs Ischemic Cardiomyopathy Heart Centre of Leipzig VT (HELP-VT) Study

Kaplan–Meier Curves for VT–Free Survival

Dinov B. Circulation. 2014;129:728-736

N=227: 63 NIDCM vs 164 ICM

VT Ablation in Nonischemic vs Ischemic Cardiomyopathy

NICM (n=63) ICM (n=164) P value

Epicardial abl, n(%) 19 (30.2) 2 (1.2) 0.0001

Noninducible PES, n(%) 9 (15.8) 14 (9.9) 0.360

Substrate mapping, n(%) 42 (66.7) 147 (89.6) <0.0001

VT induced, n/pt 2.1 ± 1.2 2.2 ± 1.3 0.744

VT mappable, n/pt 1.61 ± 0.80 1.96 ± 0.80 0.06

VT ablated, n/pt 1.40 ± 1.11 1.64 ± 1.15 0.168

Clinical VT CL (ms) 364 ± 86 385 ± 93 0.133

Procedure time (min) 181 ± 63.6 155 ± 49 0.003

Fluoroscopy time (min) 39 ± 22.4 26 ± 19 0.0001

Failure, n(%) 7 (11.1) 8 (4.9) 0.132


Catheter VT Ablation in Nonischemic vs Ischemic Cardiomyopathy Predictors of Short-term Success

Age (yr) NICM 1.02 (0.96-1.08) 0.60

ICM 0.99 (0.95-1.04) 0.82

OR; 95% CI P

ES NICM 1.98 (0.45-8.60) 0.37

ICM 0.96 (0.40-2.30) 0.922

EF% NICM 1.00 (0.94-1.07) 0.904

ICM 0.99 (0.95-1.03) 0.479

VTCL,ms NICM 1.00 (0.99-1.01) 0.47

ICM 1.00 (0.99-1.00)) 0.66

#VT NICM 0.46 (0.26-0.82) 0.008

induced ICM 0.61 (0.45-0.82)) 0.001

Epi Abl NICM 10.5 (2.52-44.0) 0.001

Incomplete success and failure Acute complete success


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Scar Progression in Nonischemic Cardiomyopathy

Berte B. J Cardiovasc Electrophysiol, 2016; 27:80-87

7 ARVC and 13 NICM: inter-procedural delay 28±18 months

Disease progression occurred in 75% of cohorts: -ventricular dilation in 45% [ARVC 71%; NICM 38%]

-decreased EF in 60% [RVEF in ARVC 71%; LVEF in NICM 54%] -scar progression in 50% [ARVC 57% and NICM 46%]

Index VT recurrence was observed in 40%. Redo ablation sites were located in previously un-ablated regions inside the index scar in 70% of patients.

Relationship of Transplant-free Survival and VT Recurrence

In patients with EF <30% and across all NYHA classes, improved transplant-free survival in those without VT recurrence

[83% vs 59%, HR 8.35], P <0.001

[93% vs 89%, HR 3.19], P =0.002

[53% vs 1%, HR 6.75], P <0.001

[96% vs 84%, HR 9.29], P <0.001

Tung et al, Heart Rhythm2015;12:1997–2007

Guidelines, Recommendations for Catheter VT Ablation

2009 EHRA/HRS Expert Consensus on Catheter Ablation of VT-2009

2015 ESC Guidelines for Management of Ventricular Arrhythmias

Structural Heart Disease

Recommended

1. Symptomatic VT despite AADs or when AADs are not tolerated. 2. Incessant VT or VT storm not due to a transient or reversible cause. 3. Frequent PVCs, NSVT associated with ventricular dysfunction. 4. Bundle branch/interfascicular VTs. 5. Recurrent polymorphic VT and VF refractory to AADs with suspected trigger

1. In patients with scar-related heart disease with incessant VT/storm 2. In patients with ischemic heart disease & recurrent ICD shocks due to VT 3. In patients with bundle branch reentrant VT 4. As additional therapy or an alternative to ICD in patients with CHD with recurrent VT or ICD therapies refractory to drug therapy.

Should be considered

1. Recurrent VT episodes despite therapy with one or more Class I or III AADs 2. VT due to prior MI, LVEF >30%, and is an acceptable alternative to amiodarone. 3. Hemodynamically stable VT due to prior MI who have LVEF ≥35% even if they have not failed AADs.

1. After first sust VT episode in patients with ischemic heart disease and ICD 2. May be considered in patients with DCM and VA not caused by bundle branch reentry refractory to medical therapy. 3. In patients with LV dysfunction associated with freq PVCs, NSVT

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Structural Heart Disease


4. May be considered in patients with Brugada syndrome with electrical storms or repeated ICD shocks.

Not recommended

For asymptomatic infrequent PVC in patients with congenital heart disease (CHD) and stable ventricular function.




No Structural Heart Disease

Recommended

1. Monomorphic VT that is causing severe symptoms. 2. Monomorphic VT when AADs are not effective,

1. In symptomatic patients with outflow tract VT failed AAD or in those with a decline in LV function due to PVC burden. 2. As first-line treatment in symptomatic patients with idiopathic left VTs. 3. PVCs triggering recurrent VF leading to ICD interventions


1. In symptomatic patients with LVOT/ aortic cusp/epicardial VT/PVC after failure of class IC agents or to avoid long-term AAD therapy 2. After failure/intolerance of class IC AAD in symptomatic patients with papillary muscle tachycardia-under echo guidance 3. In symptomatic patients with mitral and tricuspid annular tachycardia. 4. In patients with short-coupled torsade de pointes for long-term suppression/ prevention of electrical storm/ICD shock

Substrate Modification or VT Induction as the First Step?

N=48 patients: 37 ischemic cardiomyopathy, 10 NICM, 1 ARVC were randomized to:

Group 1, n=24: Substrate ablation with scar de-channeling first

Group 2, n=24: Standard VT induction, mapping, ablation first followed by scar de-

channeling

Kaplan-Meier Curves for VT Recurrence

P=0.557

Group 1 has shorter procedural parameters

compared to Group 2:

-procedure time (209±70 vs 262±63 min; P=0.009)

-fluoroscopy time (14±6 vs 21±9 min; P=0.005)

-electrical cardioversion (25% vs 54%; P=0.039)

Noninducibility of any VT was achieved in 87.5%

and 70.8% of patients (P=0.155).

VT induction and mapping before substrate

ablation prolongs the procedure, radiation

exposure, and the need for cardioversion without

improving acute results and long-term outcomes.

Fernández-Armenta J. Heart Rhythm2016;13:1589–1595

followup of 22±14 months

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Role of Early Prophylactic Catheter VT Ablation

N=98, 1/2008-4/2009, with VT and SHD:

-58% in VT storm and 67% on high dose

amiodarone.

Early referral (N=36)

Late referral (N=62): ≥ 2 episodes of VT, separated

by >1 month

In Kaplan–Meier analysis, the early referral group

had superior 1-year VT free survival (P=0.01).

Early referral

Late referral

Ischemic 63% Nonischemic 37%

Frankel DS. J Cardiovasc Electrophysiol, 2011; 22:1123.

P=0.01

(1) <30 days

(2) 30 days-12 months

(3) >12 months

Dinov B. Circ Arrhythm Electrophysiol. 2014;7:1144

HR 2 vs 1=1.85; p=0.009

HR 3 vs 1=2.04; p=0.001

N=300 cath abl of sustained VT.

-Group 1 (25%): <30 days after 1st VT

-Group 2 (28%): 30 days-12 months

-Group 1 (47%): >12 months

In Kaplan-Meier curves of VT-free survival, cath abl

within 30 days after 1st VT event is associated with

improved acute and long-term success.

Ischemic 68% Nonischemic 32%

Other Clinical Trials in VT Catheter Ablations

• ASPIRE: Early Ablation Therapy for the Treatment of Ischemic Ventricular

Tachycardia in Patients With Implantable Cardioverter Defibrillators

– stopped enrollment

• STRATUM-VT: Stepwise AppRoAch To sUbstrate Modification for Ventricular

Tachycardia


• STAR-VT: Substrate Targeted Ablation using the FlexAbility™ Ablation Catheter

System for the Reduction of Ventricular Tachycardia

– prophylactic scar-based VT ablation (both ischemic and non-ischemic)


• VANISH: Ventricular Tachycardia Ablation or Escalated Drug Therapy

– significantly lower rate of the composite outcome of death, VT storm, or appropriate ICD

shock in patients undergoing catheter ablation than those receiving an escalation in

antiarrhythmic drug therapy

• PARTITA: Does Timing of VT Ablation Affect Prognosis in Patients With an

Implantable Cardioverter-defibrillator?

VT Ablation 2016: Indications and Expected Outcomes

• Persistent inducibility is associated with VT recurrence and poor long-term results

in both NIDCM and ICM. A substrate-based, extensive ablation strategy is

associated with improved outcomes.

• Post-infarction VTs are often associated with a relatively “stable” substrate.

Catheter ablation for post-infarct VT is becoming more mainstream and not

limited to a “last-resort” strategy.

• NIDCM consists of a heterogeneous group of conditions with unknown factors

leading to modification of arrhythmia substrate over time. Disease/scar

progression is the rule. However, incomplete ablation is the most common

finding, strongly suggesting the need for more extensive ablation.

• Successful VT ablation has been associated with an mortality benefit with an

improved transplant-free survival in those without VT recurrence

• Early intervention and a “substrate ablation-first” approach may be preferable

compared to antiarrhythmic drug use and the standard VT induction protocol.

• Evolving with expanded and specific indications for VT ablations that include (1)

PVCs induced LV dysfunction, (2) Brugada syndrome with electrical storms, (3)

short-coupled torsade de pointes, (4) annular-LVOT-epicardial arrhythmias

REFERENCES: Palaniswamy C, et al. Catheter ablation of post infarction ventricular tachycardia:Ten-year trends in utilization, in-hospital complications, and in-hospital mortality in the United States. Heart Rhythm, 2014. 11(11):2056–2063. Sacher F, et al. Ventricular tachycardia ablation: Evolution of patients and procedures over 8 years. Circ Arrhythmia Electrophysiol., 2008. 1:153-161. Nakahara S, et al. Characterization of the Arrhythmogenic Substrate in Ischemic and Nonischemic Cardiomyopathy: Implications for Catheter Ablation of Hemodynamically Unstable Ventricular Tachycardia. J Am Coll Cardiol, 2010. 55(21):2355-2365. de Bakker J, et al. Slow conduction in the infarcted human heart: "Zigzag" course of activation. Circulation, 1993. 88(3):915-926. Reddy V, et al. Prophylactic Catheter Ablation for the Prevention of Defibrillator Therapy. N Engl J Med, 2007. 357:(26):2657-2665. Kuck K, et al. Catheter ablation of stable ventricular tachycardia before defibrillator implantation in patients with coronary heart disease (VTACH): A multicentre randomised controlled trial. Lancet, 2010. 375(9708):31–40. Stevenson W, et al. Irrigated Radiofrequency Catheter Ablation Guided by Electroanatomic Mapping for Recurrent Ventricular Tachycardia After Myocardial Infarction: The Multicenter Thermocool Ventricular Tachycardia Ablation Trial. Circulation, 2008. 118:2773-2782. Tanner H, et al. Catheter Ablation of Recurrent Scar-Related Ventricular Tachycardia Using Electroanatomical Mapping and Irrigated Ablation Technology: Results of the Prospective Multicenter Euro-VT-Study. J Cardiovasc Electrophysiol, 2009. 21(1):47-53. Yokokawa M, et al. Reasons for recurrent ventricular tachycardia after catheter ablation of post-infarction ventricular tachycardia. J Am Coll Cardiol, 2013. 61(1):66–73. Silberbauer J, et al. Noninducibility and late potential abolition: A novel combined prognostic procedural end point for catheter ablation of postinfarction ventricular tachycardia. Circ Arrhythm Electrophysiol, 2014. 7(3):424-435. Dinov B, et al. Outcomes in catheter ablation of ventricular tachycardia in dilated nonischemic cardiomyopathy compared with ischemic cardiomyopathy: Results from the Prospective Heart Centre of Leipzig VT (HELP-VT) Study. Circulation, 2014. 129(7):728-736. Jaïs P, et al. Elimination of Local Abnormal Ventricular Activities: A new end point for substrate modification in patients with scar-related ventricular tachycardia. Circulation, 2012. 125(18):2184-2196. Di Biase L, et al. Endo-epicardial homogenization of the scar versus limited substrate ablation for the treatment of electrical storms in patients with ischemic cardiomyopathy. J Am Coll Cardiol, 2012. 60(2):132–141.

Berruezo A, et al. Scar de-channeling: New method for scar-related left ventricular tachycardia substrate ablation. Circ Arrhythm Electrophysiol, 2015. 8(2):326-336. Santangeli et al, Indication for Ablation and Trials, Ventricular Tachycardia Ablation: A Practical Guide, 2014. CardioText Sacher F, et al. Epicardial VT ablation: A multicenter safety study. J Am Coll Cardiol, 2010. 55(21):2366–2372. Cano O, et al. Electroanatomic Substrate and Ablation Outcome for Suspected Epicardial Ventricular Tachycardia in Left Ventricular Nonischemic Cardiomyopathy. J Am Coll Cardiol, 2009. 54(9):799–808. Piers S, et al. Contrast-enhanced MRI-derived scar patterns and associated ventricular tachycardias in nonischemic cardiomyopathy: Implications for the ablation strategy. Circ Arrhythm Electrophysiol, 2013. 6(5):875-883. Oloriz T, et al. Catheter ablation of ventricular arrhythmia in non-ischaemic cardiomyopathy: Anteroseptal versus inferolateral scar sub-types. Circ Arrhythm Electrophysiol, 2014. 7(3):414-423. Dinov B, et al. Early referral for ablation of scar-related ventricular tachycardia is associated with improved acute and long-term outcomes: Results from the heart center of leipzig ventricular tachycardia registry. Circ Arrhythm Electrophysiol, 2014. 7(6):1144-1151. Berte B, et al. VT recurrence after ablation: Incomplete ablation or disease Progression? A multicentric European study. J Cardiovasc Electrophysiol, 2016. 27(1):80-87. Tung R, et al. Freedom from recurrent ventricular tachycardia after catheter ablation is associated with improved survival in patients with structural heart disease: An International VT Ablation Center Collaborative Group study. Heart Rhythm, 2015. 12(9):1997-2007. Fernández-Armenta J, et al. Substrate modification or ventricular tachycardia induction, mapping, and ablation as the first step? A randomized study. Heart Rhythm, 2016. 13(8):1589-1595. EHRA/HRS Expert Consensus on Catheter Ablation of Ventricular Arrhythmias: Heart Rhythm, 2009. 6(6):886-933. ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death: The Task Force for the Management of Patients with Ventricular Arrhythmias and the Prevention of Sudden Cardiac Death of the European Society of Cardiology (ESC). Eur Heart J, 2015. 36(41):2793-2867.

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