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Ablation of Idiopathic Ventricular Tachycardia: Endocardial and

Epicardial Approaches

Nitish Badhwar, MD, FACC, FHRS Associate Chief, Cardiac Electrophysiology

Director, Cardiac Electrophysiology Training Program University of California, San Francisco

Innovative Procedures, Devices, and State of the Art Care for Arrhythmias, Heart Failure and Structural Heart Disease

October 8, 2015

Disclosures

Honoraria - St. Jude, Biosense, Senterheart Fellowship Support – Medtronic, St. Jude, Boston

Scientific, Biotronik, Biosense Webster

•  Non-sustained ventricular tachycardia (NSVT)

–  3 or more consecutive QRS complexes of ventricular origin at rate of more than 100 bpm

•  Sustained VT –  Lasts more than 30 seconds, usually requires intervention

for termination

•  Monomorphic VT

–  Uniform QRS configuration

•  Polymorphic VT –  Beat to beat variation in QRS configuration

•  Electrical storm –  > 3 VT/VF episodes in 24 hours

Ventricular Tachycardia

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•  Sudden cardiac arrest (ventricular fibrillation)

•  Syncope, near syncope

•  Palpitations with wide complex tachycardia (hemodynamically tolerated) or frequent PVCs

Ventricular Tachycardia

1. Catheter Ablation

2. Urgent left heart catheterization

3. Start I/V Amiodarone

4. Do Nothing

What is the best treatment option?

Wide Complex Tachycardia:

Artifact

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Idiopathic Ventricular Tachycardia

•  Long QT syndrome

•  Short QT syndrome •  J wave syndromes-

Brugada, Early repolarization

•  Catecholamine induced polymorphic VT

•  Short coupled torsades

•  Outflow tract VT- RVOT VT, LVOT VT,cusp VT

•  Fascicular VT- LAF, LPF, Septal

•  Annular VT- Mitral, Tricuspid

•  VT from crux of heart

Polymorphic VT /VF Monomorphic VT

Bigeminal PVC

Holter monitor

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PVC induced Cardiomyopathy

•  Associated with high burden ( >24% Holter burden....Bogun et al)

•  Monomorphic PVCs

•  Cardiomyopathy reverses with ablation of PVC

•  Mechanism not well defined

–  ?Coupling interval

–  ?Dyssynchrony

–  ?Rate related

Coupling Interval Dispersion and BMI are Independent Predictors of PVC Cardiomyopathy

Kawamura et al. JCE..2014;25:756-62.

760 Journal of Cardiovascular Electrophysiology Vol. 25, No. 7, July 2014

Figure 4. Receiver operator characteris-tics curve analysis demonstrated. A cutoffof CI-dispersion with >99 millisecondsbest separated patients with and with-out PVC-induced cardiomyopathy. AUC= area under curve; ROC = receiver op-erator characteristics.

TABLE 2Relationship Between BMI and LV Dysfunction

LV Dysfunction Normal LV(n = 51) (n = 163) P Value

BMI < 25 (kg/m2) 15 (30%) 86 (53%) 0.0125–30 (kg/m2) 17 (33%) 56 (34%) 0.8930 (kg/m2) < BMI 19 (37%) 21 (13%) 0.001

BMI = body mass index.

TABLE 3Multivariate Analysis of Characteristics Associated with Presence of LV

Dysfunction

Odds Ratio 95% CI P Value

Age 1.014 0.981–1.043 0.392Maximum coupling interval 1.008a 0.997–1.010 0.14Coupling interval dispersion 1.045b 1.027–1.067 <0.001PVC burden 1.045 1.007–1.089 0.012QRS duration 0.992 0.971–1.014 0.592Body mass index (>30 kg/m2) 3.031 1.209–7.681 0.001

aPer 1 milliseconds increase in CI.bPer 1 milliseconds increase in CI-dispersion. BMI = body mass index;CI = confidence interval; SD = standard deviation.

LV dysfunction in adult. Longer-CI might reduce LV fillingtime for the next sinus beat. The reduced filling might ini-tiate sympathetic reflex activity leading to activation of therenin-angiotensin system and subsequent myocardial fibro-sis. However, it is unclear whether longer-CI is the cause oreffect of cardiomyopathy. Longer-CI affects the LV fillingprofile, stroke volume, and pulse pressure.17 Furthermore,longer-CI caused LV dyssynchrony, increased oxygen con-sumption and decreased LVEF. Longer-CI might, therefore,be a cause of cardiomyopathy. Smith et al.18 reported thatfrequent ventricular ectopy can increase sympathetic neuralactivity and shift the autonomic balance to a sympathetic-dominant state. Furthermore, data from a pig model Huizaret al.19 supported a causative relationship between longer-CI,

worse LV dyssynchrony, and LV dysfunction. Bradycardiahas also been suggested as a mechanism of PVC-inducedcardiomyopathy, especially in patients with a long pause fol-lowing PVCs.20,21 Sosnowski et al.22 gave support for therelationship between the longer delta-CI and LV dysfunc-tion. The standard deviation of CI and LVEF were negativelycorrelated in patients with coronary artery disease. This re-sult is similar to our study except our study has no patientswith coronary artery disease.

QRS Morphology and Duration

Neither PVC morphology nor PVC site of origin were as-sociated with reversible LV dysfunction in our study. Munozet al.8 reported that PVCs originating from the right ventriclewere associated with LV dysfunction in patients with PVCburden >10%, whereas PVCs originating from the LV wereassociated with LV dysfunction only in those with PVC bur-den >20%. Our study included PVCs with various sites oforigin, including RVOT, LVOT, LV, fascicles, and papillarymuscles. The PVCs originating from the fascicles or ventric-ular septum typically had a narrow QRS wave as opposed toPVCs originating from the free wall and nonseptal outflowtracts. Although we failed to define a clear association be-tween site of origin and the development of PVC-induced LVdysfunction, further studies with larger numbers of patientsare clearly needed to test for such a relationship. Prior studiesreported that PVC–QRS duration was associated with PVC-induced LV dysfunction,8,23 presumably because wider QRSduration was associated with worse LV dyssynchrony.24

In our study, 188 patients present monofocal PVCs and26 patients present multifocal PVCs. To derive the PVC-CI,it may be more useful of the measurement of the monofo-cal PVCs. However, we investigated the consecutive PVCsbefore we used the sedation or isoproterenol. Therefore, thisstudy included some nontarget PVCs. In patients with mul-tifocal PVCs (n = 26), the CI-dispersion for those with LVdysfunction was significant greater than as compared withnormal LV function (117 ± 23 milliseconds vs. 93 ± 15milliseconds; P = 0.001). In patients with monofocal PVC(n = 188), the CI-dispersion for those with LV dysfunction

I II III

aVL

aVF V1 V2

V3

V5 V6

V4

aVR

Right Ventricular Outflow Tract VT(RVOT VT)

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Pulmonary valve

Tricuspid valve

Ablation site

Differentiating ARVC from RVOT

Hoffmayer, et al. Heart Rhythm..2013;10(4):477-82

Lead 1 QRS> 120 ms QRS Transition at V5 Notching QRS complex Anterior T wave inversion in sinus rhythm

Left Aortic Cusp VT

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Left main coronary artery

Ablation catheter

Left Aortic Cusp VT

Aortic Cusp VT ECG Criteria

•  Early transition in precordial leads (V1, V2)

•  Notch in V5, lack of S in V5, V6 •  Broad R wave and larger R/S in V1, V2 •  Variable coupling interval of PVC •  PVC transition compared to sinus rhythm

transition •  Phase analysis (as measured from earliest

surface onset) –  Local onset in V2 ≥ 7 ms –  Initial peak / nadir in III ≥ 120 ms –  Initial peak / nadir in V2 ≥ 78 ms

Daniels D V et al. Circulation 2006;113:1659-1666

EKG criteria for epicardial VT: Precordial MDI

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Epicardial Outflow Tract VT

Epicardial outflow Tract VT

CS  

Epi  

Epi  

CS  

Epicardial Outflow Tract VT

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Surgical Epicardial Ablation for Outflow Tract VT

Outflow Tract VT

Fascicular VT

•  Induction with atrial pacing •  RBBB, LAD •  No structural heart disease (Zipes,

1979) •  Verapamil sensitive (Belhassen,

1981) •  RBBB, RAD (Ohe, 1988) •  Upper septal (Shimoike, 2000)

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Left Posterior Fascicular VT

Badhwar N, Scheinman MM. Curr Probl Cardiol. 2007;32(1):7-43

Left Anterior Fascicular VT

Left Ventricular Upper Septal VT

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300 Journal of Cardiovascular Electrophysiology Vol. 24, No. 3, March 2013

Figure 2. VT morphologies and corre-sponding circuits in Case 4. (A) Left pos-terior fascicular VT morphology prior toablation at outside institution. The cir-cuit includes retrograde conduction upthe septal fascicle (S) and antegrade con-duction down the posterior fascicle (P),with passive activation of the right bundlebranch (RBB) and likely slow conductiondown the anterior fascicle (A). (B) VT1with narrow QRS and right axis devia-tion. The circuit involves retrograde con-duction up S and antegrade conductiondown A, with likely block in P. Passive ac-tivation of RBB is still present accountingfor the narrow QRS. (C) VT2 with RBBBand right axis deviation. The circuit is thesame as in B, with either block or sig-nificant delay in the RBB accounting forthe new RBB block morphology in com-parison to 2B. (D) VT3 with left bundlebranch block and left superior axis. Thecircuit here is bundle branch reentry, withretrograde conduction likely up S and an-tegrade conduction down RBB.

the left anterior fascicle (LAF) and LPF in at least 1 VTform, and retrograde conduction over LAF or LPF was notobserved for any VT forms. In Case 1, pacing from the LPFfor RBBB LS axis VT resulted in concealed entrainment withPPI within 30 milliseconds of TCL (PPI = TCL). In Case 4,pacing from LAF during RBBB RI axis VT resulted in nearconcealed entrainment with PPI equal to TCL. However, inall 4 cases, entrainment just distal to the left bundle branch(LBB) anatomically between the LPF and LAF resulted inconcealed (or near concealed) entrainment with PPI equal toTCL with S–QRS equal to FP–QRS.

Cases 5 and 6 exhibited spontaneously shifting VT mor-phologies, from RBBB LS to RBBB RI axis. Although en-trainment from the left sided fascicles was not performed inCase 5, entrainment from the proximal LAF in Case 6 re-sulted in PPI equal to TCL and concealed entrainment withalternation of VT morphologies to match the 2 clinical mor-phologies.

Sites of Successful Ablation

Empiric or targeted ablation based on entrainment crite-ria of the mid LPF was initially performed in Cases 1–5 forRBBB LS axis VT. If there was no affect on tachycardia,ablation was extended to the proximal LPF. In all 5 cases,ablation of the LPF terminated RBBB LS axis VT, but re-sulted in inducible RBBB/narrow complex RI axis VT orRBBB, RI axis. Successful ablation of tachycardia for Cases1–3 was performed just apical to the LBB, anatomically be-tween the LPF and LAF. In Cases 4 and 5, proximal LAFablation was performed after LPF ablation, but resulted inLBBB in SR as well as LBBB VT. In Case 4, LBBB VT wasproven bundle-to-bundle reentry tachycardia (BBRT) basedon all the usual criteria, but with a relatively short HV inter-val in BBRT (36 milliseconds) versus SR (60 milliseconds)(see “Discussion”). Further ablation in Case 4 was not per-formed and the patient was placed on medical therapy with

Sung RK, et al. JCE..2013;24:297-304.

Multiform

Fascicular VT

a. Anterolateral

b. Posterior

c. Posteroseptal

Mitral Annular VT

1 Septal a.  Qs in V1

b.  Narrower

c.  No notching

2. Lateral a.  rS in V1

b.  Wider

c.  Notching

Tricuspid Annular PVCs / VT

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•  Rapid VT, can present as electrical storm

•  Exercise induced / require isoproterenol for induction

•  Hemodynamic collapse •  Responds to beta-blockers, lidocane •  Catheter ablation is curative

Idiopathic VT arising from Cardiac Crux

Kawamura M et al. Circ Arrhythm Electrophysiol. 2014;Sep 15 (Epub)

Cardiac Crux

•  Cardiac crux is the intersection between the AV, posterior inter-ventricular and inter-atrial grooves

 

Kawamura M et al. Circ Arrhythm Electrophysiol. 2014;Sep 15 (Epub)

Idiopathic VT arising from Cardiac Crux

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PVC/VT: QS in lead II and/or III, R > S in lead V2 and MDI ≧ 0.55

RBBB pattern LBBB pattern

R < S in lead V6

Apical crux-VA

LV posteroseptal mapping

Epicardial surface mapping using subxiphoid approach

R < S in lead V6

Apical crux-VA

Middle MCV mapping

Epicardial surface mapping using subxiphoid approach

YES

Basal crux-VA

1) Proximal-CS mapping 2) Proximal MCV mapping

NO

Idiopathic VT from Cardiac Crux

Kawamura M et al. Circ Arrhythm Electrophysiol. 2014;Sep 15 (Epub)

RAO

LAO

Basal crux site Apical crux site Epicardial ablation Proximal MCV ablation

CS RCA

CS

ABL

ABL

RCA

ABL

RCA

ABL

Idiopathic RBBB LAD VT

•  Fascicular VT –  rS in II, III, avF –  MDI <0.55

•  Papillary muscle VT –  Can have QS in II, III, qR in V1, QRS >150 ms –  Rarely MDI > 0.55

•  Crux VT –  QS in II, III –  QS or r/S in V6, R in avR, MDI >0.55

Kawamura M et al. Heart Rhythm. 2015 (Epub)

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Exercise Induced Ventricular Tachycardia

Pace map

VT Epi Endo

Pellegrini CN, Scheinman MM, Badhwar N. J Electrocardiol. 2011; 44: 792-5.

Successful Epicardial Site of Ablation

Pellegrini CN, Scheinman MM, Badhwar N. J Electrocardiol. 2011; 44: 792-5.

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Coronary Anatomy

Pellegrini CN, Scheinman MM, Badhwar N. J Electrocardiol. 2011; 44: 792-5.

•  Idiopathic monomorphic VT usually arises from

outflow tract, fascicles, annulus or Crux and can be epicardial in origin

•  ECG characteristics can localize the site of origin of VT and guide catheter ablation

•  Treatment –  Monomorphic VT / Frequent PVCs curable with

catheter ablation –  Polymorphic VT treated with ICD and drugs

Conclusion-Idiopathic VT

•  Outflow tract VT can arise along the course of

AIV, GCV, LAD

•  Epicardial VT arising from the crux along the course of MCV

•  Uncommon origin along the lateral LV (remote from vascular structures)

•  Excellent response to epicardial ablation

Conclusion-Epicardial Idiopathic VT