Supraventricular Tachycardias

AV Nodal Reentrant Tachycardia (AVNRT)

AVNRT
AVNRT Features Pts usually young to middle aged adults More common in females Concentric (septal) retrograde atrial activation low to high Pseudo R wave in V1 Dual AV Nodal physiology common (fast and slow pathways) Tachycardia is AV nodal dependent and is usually 1:1 AV conduction Shortest VA during tachycardia is < 60 ms

Baseline ECG

AVNRT 12 Lead: Pseudo R Wave

AVNRT

Sinus Rhythm

AVNRT

AV Nodal Jump With an Echo

S1(A1)

S1(A1)

S2(A2)

echo A
H V A H V

230 ms increase in AH to 450 ms jump

(FPWERP and jump to SPW)

AVNRT Induction

JUMP(FPERP) Long AH Interval Up Fast Down Slow PW

ECHO

UF DS DS

UF

Sustained AVNRT

Sustained AVNRT

AVNRT Terminates with Adenosine

Atrial Pacing Protocol

Exercise: What is happening here? Which catheter is being paced? Is it capturing? How many extras are given? Is an arrhythmia induced? What happens to the AH interval?

Atrioventricular Reciprocating Tachycardia (AVRT)Concealed Bypass Tracts and WPW

Accessory AV Pathways
APs represent an extra connection outside the AV Node Concealed pathways have only retrograde conduction and do not have pre-excitation (NO delta wave in SR) Manifest show antegrade conduction (delta wave in SR) These patients represent 30% of all SVTs.

AVRT
AVRT Features Hx of tachycardia typically beginning in childhood to young adult More common in males Concentric (septal) or eccentric retrograde atrial activation low to high Tachycardia dependent on the AV node and the ventricles; cannot continue in the presence of AV nodal or VA block Atrial preexcitation when his refractory proves AP VA during tachycardia is > 60 ms APs do not typically exhibit decremental conduction

AVRT

Nature of AVRT
May be orthodromic: down the AV node and up the accessory pathway resulting in narrow complex (90%)

May be antedromic: down the AP and up the AV node resulting in wide complex (10%)

AVRT: Manifest AP

AVRT: Manifest AP ERP

AVRT: Orthodromic

Down AV Node Up AP

Down AV Down AV Node Up AP Node

Up AP

Anatomic Locations Accessory Pathways

Septal

Free Wall Lateral

AVRT: Orthodromic via L sided AP

AVRT: AF With Pre-excitation

AVRT: Ablation of Manifest AP

AVRT: Manifest AP Delta Algorithm

* * * * * *

Algorithm for AP Identification

* *
II, III, I + and AVF + AVF -

Algorithm for AP Identification

General Concepts for Manifest Pathways

If Delta Wave Is

Then
Pathway is L sided Pathway is R sided Pathway is anterior Pathway is posterior In a vein (CS) or epicardial Pathway is left lateral Pathway is septal Multiple pathways may be present

* * * * * * * *

Positive in V1 Negative in V1 Positive in the inferior leads (II, III, AVF) Negative in the inferior leads (II, II, AVF) Negative in lead II Negative in the lateral leads (I and AVL) Making a to + transition V1 to V2 Not meeting the above criteria

The analysis of the delta wave polarity should occur during the first 25 ms of the manifest QRS complex.

AVRT

What is happening here? What is the rhythm? Where is the shortest VA time? Where is the AP?

AVRT

Using the delta wave algorithm, where is this AP located?

Diagnosing Septal Pathways Para-Hisian Pacing:

Why and How

Why
Used to distinguish mid or anteroseptal accessory pathway from AV node when retrograde conduction is concentric. Is that over the node or pathway?

How
Pacing output rather than mere electrode location is used to capture different structures.particularly the HIS bundle. Stimuli delivered to the RV septum, distal to the His recording and proximal to the right bundle recording. Pacing with high output to capture the His bundle directly (narrower QRS), then decrease output to no longer capture the His bundle (wider QRS), but depolarize the ventricle from the high septum (capture only of local ventricular myocardium)

High Output His Capture (No AP)

Capture of the HIS bundle directly will spread the impulse to the AV node retrograde and to the ventricles over the HPS=narrower QRS

Pace

Lower output: No His Capture (No AP)

His not captured as output reduced, but ventricle is depolarized from the high septum yielding a left bundle branch block QRS morphology (wider QRS). Impulse travels to apex then retrograde to His-purkinje system to the atrium so the stim to atrial depolarization time is increased (no AP present)

Pace

Anteroseptal Accessory Pathway

In the presence of an AP, the retrograde activation is rapid regardless of the activation of the HPS system or ventricular septum (occurs with narrower or wider QRS)

Pace

Para-Hisian pacing - No AP (1)

Para-Hisian pacing demonstrating retrograde conduction over the fast AV nodal pathway (AVN/AVN pattern) in a patient with AVNRT. The pacing stimulus (S) in the left complex did not produce HB-RB capture, reflected by the wide QRS complex and relatively late His bundle activation (S-H=60 ms). HB-RB capture was achieved in the right complex reflected by narrowing of the QRS complex and shortening of the S-H interval to 15 ms. The 45-ms shortening in S-H interval was matched by a 45 ms shortening in the S-A interval from 90 to 45 ms, without a change in the atrial activation sequence. The constant H-A interval (35 ms) and atrial activation sequence indicate that retrograde conduction was dependent on activation of the His bundle and not on the local ventricular myocardium and thus no AP

Wider QRS: HB/RB not activated;Late His Activation S-H=60 ms

Narrower QRS: HB/RB activated; S-H shortens to 15 ms; H-A constant; 45 ms in S-H= 45 ms in S-A w/o change in atrial activation

Para-Hisian pacing - No AP (1)

Wider QRS Narrower QRS

Wider QRS: HB/RB not activated;Late His Activation S-H=60 ms

Narrower QRS: HB/RB activated; S-H shortens to 15 ms; H-A constant; 45 ms in S-H= 45 ms in S-A w/o change in atrial activation

Para-Hisian Pacing No AP (2)

Narrower QRS Para-Hisian pacing demonstrating retrograde conduction over the slow AV nodal pathway (AVN/AVN pattern). The pacing stimulus (S) in the left complex resulted in ventricular capture and HB-RB capture, producing a relatively narrow QRS complex and early activation of the His bundle (H). HB-RB capture was lost in the right complex, resulting in widening of the QRS complex and a 60-ms increase in the S-H interval from 10 to 70 ms. This was also associated with a 60-ms increase in the S-A interval from 120 to 180 ms, without a change in the retrograde atrial activation sequence. The constant H-A interval (110 ms) and atrial activation sequence indicate that retrograde conduction was dependent on His bundle activation and not on local ventricular activation, indicating retrograde conduction exclusively over the AV node. Earlier atrial activation in the proximal coronary sinus electrogram (CSp) than in the His bundle electrogram (HBp) suggests retrograde conduction over the slow AV nodal pathway. Narrower QRS: HB/RB This tracing was recorded after ablation of a left activated; S-H short=10 lateral accessory AV pathway. ms; S-A=120 ms

Wider QRS

Wider QRS: HB/RB not activated;Late His Activation; S-H + by 60 ms (10 to 70 ms); S-A + by 60 ms (120 to 180 ms); Constant H-A (110) and A activation =His dependent activation, not local V myocardium and no AP; retro SPW (CS early)

Para-Hisian Pacing No AP (2)

Narrower QRS

Wider QRS

HA 110

HA 110

Narrower QRS: HB/RB activated; S-H short=10 ms; S-A=120 ms

Wider QRS: HB/RB not activated;Late His Activation; S-H + by 60 ms (10 to 70 ms); SA + by 60 ms (120 to 180 ms); Constant H-A (110) and A activation =His dependent activation, not local V myocardium and no AP; retro SPW (CS early)

AP Present (1)
Para-Hisian pacing demonstrating retrograde conduction only over an anteroseptal accessory AV pathway (AP/AP pattern). HB-RB capture in the left complex resulted in an S-H interval of 15 ms. Loss of HB-RB capture in the right complex resulted in a 55ms increase in S-H interval to 70 ms. The S-A interval remained fixed at 95 ms and the atrial activation sequence remained identical, indicating that retrograde conduction was dependent on the timing of ventricular activation and not on the timing of retrograde Hisbundle activation.

Narrower QRS

Wider QRS

Narrower QRS: HB/RB Wider QRS: Loss of HB/RB; S-H + by 55 ms to capture; S-H=15 ms 70 ms; S-A remains constant at 95 ms (if S-A

dependent on H, S-A would also + by 55 ms not the case here; A activation unchanged; A activation dependent on V activation, not retro H activation; thus AP present

AP Present (1)
Narrower QRS

Wider QRS

HA 65

HA 25

Narrower QRS: HB/RB capture; S-H=15 ms

Wider QRS: Loss of HB/RB; S-H + by 55 ms to 70 ms; S-A remains constant at 95 ms (if S-A dependent on H, S-A would also + by 55 msnot the case here; A activation unchanged; A activation dependent on V activation, not retro H activation; thus AP present

AP Present (2)

Narrower QRS

Wider QRS

The SA intervals and retrograde atrial activation sequence are unchanged, indicating retrograde conduction over a single accessory pathway.

AP Present (2)

Narrower QRS

Wider QRS

The SA intervals and retrograde atrial activation sequence are unchanged, indicating retrograde conduction over a single accessory pathway.

Diagnosing Septal Pathways Para-Hisian Pacing:

Summary: Wider QRS/Long S-H= Local Ventricular Capture Only Narrower QRS/Short S-H= His/RB Capture Shortening of S-H interval reflects His/RB capture S-A changes which follow S-H changes= Retro AV Node conduction S-A intervals which are short regardless of a narrower or wider QRS and which do not follow changes in the S-H interval are indicative of an AP

Effects of Bundle Branch Block During Orthodromic Tachycardia

In orthodromic AVRT with a LBBB and a left sided (here left lateral) AP, the circuit can only return to the AP via the right bundle and conduction via the left ventricular septumtherefore the VA time and the cycle length of the tachycardia is increased. This occurs only when the block is on the same side as the AP-otherwise known as ipsilateral BBB.

Normal Orthodromic

LBBB

L Lat AP=Fixed TCL and VA Time w/ Narrow QRS

L Lat AP= + TCL and VA Time w/ LBBB Netter Images

In orthodromic AVRT and a RBBB, neither the V-A time, nor the tachycardia cycle length is affected in the case of a left sided (here left lateral) AP. Only a right sided pathway would be affected by a RBBB. Ipsilateral (same side) bundle branch blocks increase the VA time and tachycardia cycle length, while a contralateral (opposite side) BBB does not.

L Lat AP= No change in TCL and VA Time w/ RBBB

Netter Images

RBBB during orthodromic AVRT using a R sided AP influences the VA interval and tachycardia cycle length. Panel (A) shows SVT with a narrow complex QRS, VA=105 ms, and a TCL=350 ms. Panel (B) shows tachycardia with a RBBB, VA increases to 180 ms, and the TCL to 425 ms.

A.

B.

105

180

RFW AP=Fixed TCL and VA Time w/ Narrow QRS

RFW AP= +TCL and VA Time w/ RBBB

Effects of Bundle Branch Block During Orthodromic Tachycardia

Summary: Narrow QRS (HPS)= BL TCL and VA time Ipsilateral (same side) BBB= + TCL and VA time Contralateral (opposite side BBB)= no change TCL or VA time LBBB: RBBB:

Classic Atrial Flutter

Atrial Flutter
What is it? Atrial flutter is a cardiac arrhythmia characterized by beat-to-beat uniformity of cycle length, polarity, and amplitude of the electrogram recordings. Atrial rates usually 200-300 beats/min.

Typical Atrial Flutter

Mechanism: Reentry, involving a large reentrant circuit localized within the right atrium, around anatomical obstacles. Involves the TVA, CS, ER and CSTA
May be counterclockwise Or clockwise
C S T A

C S T A

Counterclockwise Typical Atrial Flutter

Typical Sawtooth Flutter Waves

Intracardiac Electrograms of Typical Counterclockwise Atrial Flutter

 C. R. Bard, Inc.

 C. R. Bard, Inc.

 C. R. Bard, Inc.

 C. R. Bard, Inc.

 C. R. Bard, Inc.

 C. R. Bard, Inc.

Typical Atrial Flutter

A zone of slow conduction exists between the tricuspid annulus, coronary sinus ostium, and inferior vena cava (the isthmus) These conduction barriers are used as a guide to ablation. Pacing from this area will entrain the tachycardia and prove the mechanism. If the activation sequence during pacing is the same as flutter and the post pacing interval equals the tachycardia CL, then this is concealed entrainment.

Principles of entrainment to identify reentry circuit

An electrophysiologic technique in which pacing is used to continuously reset a reentrant circuit Identifies a wavefront that rotates around an inexcitable obstacle which, in the case of flutter, is the tricuspid valve, IVC and area of functional block along the crista terminalis Requires area of slow conduction that delays the impulse sufficiently such that it does not catch up with refractory tail of the preceding beat.

General Definition of Entrainment: A premature impulse invades the circuit during tachycardia
With correct timing, a paced impulse will divide in two, with the antidromic wavefront colliding with and extinguishing one portion of the original circuit, and the orthodromic creating a new wavefront propagating via the tachycardia pathway, and resetting it. Consists of a continuous pacing train, slightly faster than the tachycardia cycle length. Each paced impulse will advance the circuit otherwise known as entrainment.

New circuit started here

Entrainment
The goal of entrainment is to determine the relationship of a given site to the reentrant circuit There are two types of entrainment: Concealed Entrainment: entrainment without fusion (No change in P wave, QRS, or IC morphology) Manifest Entrainment: entrainment with fusion (A change in P wave, QRS, or IC morphology)

Criteria for concealed entrainment

P wave, QRS, or IC morphologies and activation sequences during pacing resemble those in tachycardia A post-pacing interval within 20-30 msec of the tachycardia cycle length recorded at the pacing site A stimulus to P, QRS, or IC signal interval equal to the electrogram to P, QRS or IC interval during tachycardia

Typical Atrial Flutter: Concealed Entrainment

Pacing during flutter Post pacing interval=tachycardia cycle length

Concealed Entrainment -PPI

Concealed Entrainment
No change in the morphology
ECG 1 ECG 2 ECG 3 LEAD 1 LEAD 2

Pacing at a slightly faster rate

Pacing at the critical site of the tachycardia

Entrainment
Concealed:
Pacing Site

Criteria for manifest entrainment (with fusion)

P wave, QRS, or intracardiac morphologies and activation sequences during pacing do not resemble that of tachycardia A post-pacing interval greater than the tachycardia cycle length by more than 20-30 msec recorded at the pacing site (the greater the PPI above the TCL, the farther from the circuit) A stimulus to P, QRS, or IC electrogram interval during pacing is not equal to the local electrogram to P, QRS, or IC interval in tachycardia

Entrainment
With Fusion:
Pacing Site

Manifest Entrainment (with fusion)

Entrainment With Fusion

Change in the morphology
ECG 1 ECG 2 ECG 3 LEAD 1 LEAD 2

Pacing at a slightly faster rate

Pacing at site non-critical to the tachycardia

Typical Atrial Flutter

Atrial flutter is cured by performing a drag ablation from the tricuspid annulus to the eustachian ridge (IVC) May also make additional line from TVA to CS or CS to ER The goal is to connect non conducting tissues to form a barrier across the isthmus.

Typical Atrial Flutter

Pacing from the CS ostium is done when patient is not in flutter to show activation sequence.

CS pacing: No isthmus block pre ablation

Typical Atrial Flutter

Pacing from the CS ostium is done after ablation to show unidirectional conduction block.
Clockwise block

Pacing lateral to the ablation line will confirm bidirectional conduction block.
Counterclockwise block

Typical Atrial Flutter

C. R. Bard, Inc.

What is happening? What is the activation sequence? What is the rhythm? What do you think of the surface EKG?

Typical Atrial Flutter

What is happening? What rhythm is on the left hand side of the tracing? What is happening to the right of the tracing?

Atrial Tachycardia

Atrial Tachycardia (A tach)

Accounts for <5% of all SVTs A tach is defined as an ectopic automatic atrial focus firing faster than the normal intrinsic rate of the sinus node Usually has different P wave morphology than sinus, although may be similar if close to the SA node Tend to be automatic in nature and are independent of the ventricle Common sites are crista terminalis, cs os, pulmonary veins, and the tricuspid and mitral annuli (although may originate anywhere)

Atrial Tachycardia

a tach

sinus

RSPV Atrial Tach PA View

Earliest Mapping Site

Atrial Tachycardia

Atrial tachycardia: More A signals than V

Earliest Site: Pre P-Wave 45 ms

45ms

Atrial Tachycardia

What rhythm is shown here? Which a is earliest? Where may this tachycardia be coming from?

Atrial Fibrillation

Atrial Fibrillation (A Fib)

Among the most prevalent SVTs Chaotic electrical pattern in the atria Negates the physiologic benefit of AV synchrony Foci from the pulmonary veins, SVC, Vein of Marshall, and other sources may serve as triggers for AF

LSPV Mapping

PV Mapping CS Pacing
S A and PVP Fusion A PVP

CS 3/4

Atrial Fibrillation: Chaotic Electrograms

Note the chaotic electrograms during a fib There is no consistent activation sequence or cycle length

Atrial Fibrillation

What is this rhythm? What is the activation sequence? Where is the earliest a?

Ventricular Tachycardias

Differential Diagnosis for VT

His-Purkinje System Tachycardias oBundle Branch Reentry Ventricular Tachycardia oVerapamil-Sensitive Left Ventricular Tachycardia oFocal His-Purkinje Tachycardia Arrhythmogenic Right Ventricular Dysplasia RVOT Ventricular Tachycardia Right ventricular scar after surgical repair of congenital heart disease Coronary artery disease with previous myocardial infarction LVOT Ventricular Tachycardia Verapamil-Sensitive Left Ventricular Tachycardia VT associated with Tetralogy of Fallot Repair

Structurally Normal Heart VT

LVOT Ventricular Tachycardia RVOT Ventricular Tachycardia Long QT Syndrome Brugada syndrome Catecholinergic VT Verapamil-Sensitive LV VT

Ventricular Tachycardia (VT)

VT Features VT originates from the ventricle The atrium and AV node are dissociated from the ventricle 2 types are idiopathic and ischemic Idiopathic VT is from a normal heart, is focal, and is usually non-life threatening Ischemic VT comes from coronary disease, is reentrant, and associated with an MI--tends to be more life threatening due to a low EF.

Strategy for Catheter Ablation of VT

Focal Mechanism Target Tools
Triggered Activity Automaticity Ablate Focus

Macroreentry
Intra myocardial Re entry Ablate Critical Pathway

-Analysis of 12 lead ECG -Analysis of 12 lead ECG of VT of VT -Pace mapping -Pace mapping Response to pacing (PPI and
CE)

-Activation mapping

-Activation mapping -Substrate Mapping (Voltage Mapping)

Idiopathic VT
Most commonly from RVOT; other sites also possible Associated with a normal heart; usually benign Reproducibility unpredictable with pacing: burst pacing may trigger as this is primarily an automatic rhythm, not reentrant Pts typically receive ablation or medical therapy

IDIOPATHIC VENTRICULAR TACHYCARDIA

RIGHT VENTRICLE

LEFT VENTRICLE

RVOT

80%
PAROXYS MAL EXERCISE INDUCED

FASCICLES

15%

NON-SUSTAINED

ANTERIOR

POSTERIOR

VT

SUSTAINED VT
RBBB RIGHT AXIS NARROW QRS RBBB LEFT AXIS NARROW QRS

LBBB INFERIOR AXIS

5% other locations

Idiopathic RVOT VT from a young male with a normal heart. The QRS is wide, and regular (.14 sec). There is a left bundle branch pattern (QRS negative in V1) and an inferior axis (QRS positive in II, III, and AVF). Independent P waves are not apparent.

RVOT VT and Automaticity

RVOT VT: Mapping Catheter in RVOT

VA Dissociation Proves VT Mechanism

RVOT VT: Mapping EGM 33

Early site in RVOT

Pacemapping RVOT VT. Clinical VT is on left. A-E show single paced complexes from five different sites attempting to match VT QRS. In A-D, the QRS appears progressively more similar to the target morphology: successful ablation occurred at site E, where pacing creates a perfect 12/12 perfect EKG pace map.

12/12 Pace Map: Side By Side Comparison

Perfect Pace Map

VT

In a pt with a normal heart, this VT is induced. Where in the heart do you think it is coming from?

Idiopathic Left Ventricular Tachycardia

Left Fascicular VT -reentry or triggered Left Ventricular Outflow Tract VT -automatic

LVOT VT. CL=290 ms; RBBB morphology (+) V1. Inferior Axis (+) II, II, and AVF. Precordial leads are concordant with a positive, peaked QRS.

Left Ventricular Outflow Tract VT

Three locations possible 1. Endocardial 2. Coronary cusp 3. Epicardial

Ventricular ectopy arising from the base of the left coronary cusp.

Left Fascicular VT
Also known as verapamil sensitive VT
Left Posterior fascicular VT with a RBBB and superior axis(common) Left Anterior fascicular VT with a RBBB and right axis(uncommon) Upper septal fascicular VT with a narrow QRS and normal axis(rare

Young patients without heart disease Posterior and anterior fascicular VT can be successfully ablated at the mid-septum guided by a diastolic Purkinje potential or at the VT exit site guided by a fused pre-systolic Purkinje potential

Left Posterior Fascicular VT

Right bundle (positive (+) V1) superior axis (II, III, and AVF negative (-))

Left Posterior Fascicular VT

Fused pre-systolic Purkinje potential

Ischemic VT
Induced with PES Re-entry in nature RF is second line therapy Stable Vs Unstable VT

Ischemic VT

What is happening here? What is the rhythm? Is there association between the A and V? What is the activation sequence?

Ischemic VT

Ischemic VT

v v v

Ischemic VT
Associated with scar from a myocardial infarction through which a reentry circuit rotates 90% inducible in EP lab with programmed stimulation Pts typically receive ICD/ablation is 2nd line therapy for patients receiving frequent shocks

VT circuit in scar

Substrate Mapping - Voltage

EGM amplitude > 1.5 mV ; normal myocardium EGM amplitude 0.5 1.5 mV ; border zone EGM amplitude < 0.5 mV; dense scar
Marchilinski et al Circ 2000, Reddy 2004

LV - RAO
>1.5mV

LV - LAO

< 0.50mV

LV - PA

LV - BOTTOM

980528RM

Endocardial Scar / Infarct Size: Magnetic Mapping - 37% Vs SPECT Imaging - 36%

Ischemic VT: Scar Voltage Mapping

Electrically Unexcitable Scar

Pace at 10 mA unipolar from map catheter If there is failure to capture, then the area is tagged as scar Can be used to identify borders of low voltage infarct regions and borders of infarct zones Can identify areas that will NOT respond to RF as they are already electrically inert

Ventricular Tachycardia

Ventricular Tachycardia (VT)

VT Features VT originates from the ventricle The atrium and AV node are dissociated from the tachycardia AV dissociation is often seen during VT 2 types are idiopathic and ischemic Idiopathic VT is from a normal heart, is focal, and is usually non-life threatening Ischemic VT comes from coronary disease, is reentrant, and associated with an MI--tends to be more life threatening due to a low EF.

Ischemic VT
Most common type of VT Usually LV; life threatening if EF is low Associated with scar from a myocardial infarction through which a reentry circuit rotates 90% inducible in EP lab with programmed stimulation Pts typically receive ICD/ablation is 2nd line therapy for patients receiving frequent shocks

VT circuit in scar

Ischemic VT

Ischemic VT

v v v

Ischemic VT: Scar Voltage Mapping

Electrogram recorded from the LV endocardium during VT in a patient with a prior MI. A isolated low amplitude mid-diastolic potential precedes local ventricular activation by approximately 150-160 ms. This potential presumably reflects activation of a zone of slow conduction. Ablation in such a site may successfully result in VT termination.

Ischemic VT

What is happening here? What is the rhythm? Is there association between the A and V? What is the activation sequence?

Idiopathic VT
Represents the minority of all VTs Most commonly from RVOT; other sites also possible Associated with a normal heart; usually benign Reproducibility unpredictable with pacing: burst pacing may trigger as this is primarily an automatic rhythm, not reentrant Pts typically receive ablation or medical therapy

IDIOPATHIC VENTRICULAR TACHYCARDIA IDIOPATHIC VENTRICULAR TACHYCARDIA

RIGHT VENTRICLE RIGHT VENTRICLE

LEFT VENTRICLE LEFT VENTRICLE

RVOT RVOT

80%
PAROXYS MAL PAROXYS MAL EXERCISE INDUCED EXERCISE INDUCED

FASCICLES FASCICLES

15%

NON-SUSTAINED NON-SUSTAINED

RMVT RMVT

ANTERIOR ANTERIOR

POSTERIOR POSTERIOR

SUSTAINED VT SUSTAINED VT

LBBB LBBB INFERIOR AXIS INFERIOR AXIS

RBBB RBBB RIGHT AXIS RIGHT AXIS NARROW QRS NARROW QRS

RBBB RBBB LEFT AXIS LEFT AXIS NARROW QRS NARROW QRS

5% other locations

Idiopathic RVOT VT from a young male with a normal heart. The QRS is wide, and regular (.14 sec). There is a left bundle branch pattern (QRS negative in V1) and an inferior axis (QRS positive in II, III, and AVF). Independent P waves are not apparent.

RVOT VT and Automaticity

RVOT VT: Mapping Catheter in RVOT

VA Dissociation Proves VT Mechanism

RVOT VT: Mapping EGM 33

Early site in RVOT

Pacemapping RVOT VT. Clinical VT is on left. A-E show single paced complexes from five different sites attempting to match VT QRS. In A-D, the QRS appears progressively more similar to the target morphology: successful ablation occurred at site E, where pacing creates a perfect 12/12 perfect EKG pace map.

12/12 Pace Map: Side By Side Comparison

Perfect Pace Map

VT

In a pt with a normal heart, this VT is induced. Is is ischemic or idiopathic? Where in the heart do you think it is coming from?

Bundle Branch Reentrant Ventricular Tachycardia

VT From Bundle Branch Reentry

Occurs in up to 30% of VT associated with idiopathic dilated cardiomyopathy VT is usually left bundle branch block (negative QRS in V1), superior axis (negative QRS in II, III, and AVF) morphology

VT From Bundle Branch Reentry

Dependent on both bundles for reentry Baseline EKG usually will demonstrate signs of underlying conduction delay (bundle branch block) and signs of cardiac dilatation (atrial enlargement)

Goals: Ablate right bundle and abolish reentry

Baseline Sinus EKG in BBRVT

The baseline sinus rhythm EKG demonstrates a classic LBBB (wide negative QRS in V1>120 ms) with left atrial enlargement as seen with a large negative component to the P wave in V1 and a very broad P wave in lead II.

VT Due to Bundle Branch Reentry

The EKG of bundle branch reentry VT demonstrates a left bundle branch block pattern (wide negative QRS in V1) with a superior axis (negative QRS in II, III, and AVF).

VT Due to Bundle Branch Reentry

The typical induction method for BBRVT is with single premature beats from the right ventricle. Here, a single premature beat (S) blocks retrograde in the right bundle branch, but conducts up the left bundle branch into the His Bundle.

His Bundle Right Bundle Branch Left Bundle Branch

VT Due to Bundle Branch Reentry

Often, by the time the impulse gets up the left bundle and through the His, the right bundle has recovered and the impulse then travels antegrade down the right bundle branch, then back up the left bundle, initiating the reentry circuit of bundle branch reentry with a LBBB pattern. The His is part of the circuit and a 1:1 relationship is observed between the His and V during VT.

His Bundle Right Bundle Branch Left Bundle Branch

In rare instances, the premature beat may block in the left bundle retrograde and set up a circuit in the reverse direction with a RBB pattern (wide positive QRS in V1)

Baseline HV in BBRVT
It is quite typical to observe a baseline prolonged HV interval in patients with BBRVT during sinus rhythm. In this example the baseline HV is slightly prolonged at 65 ms.

VT EKG in BBRVT
Interestingly, the EKG during BBRVT shows a similar QRS morphology as compared to the baseline sinus EKG: a classic LBBB. With careful inspection, VA dissociation may also be observed at the rhythm strip on the bottom as P waves march through the QRS.

VA Dissociation in BBRVT
During BBRVT, there is a left bundle branch pattern and a dissociation between the V and A signals. The A signals are not only dissociated as they march through the VT, they are high to low, denoting a sinus origin.The atrial dissociation demonstrates the atrium is not part of the circuit.

Negative QRS (LBB pattern) in V1 during VT

HRA

The As Walk Through The Vs

The Atrial Activation is High to Low

V-His Association in BBRVT

While the A is dissociated, each V is preceded by a His signal denoting the His is part of the circuit. This is diagnostic for BBRVT. In addition, the HV in BBRVT, as seen here, is classically > 100 ms.

HRA

HV Interval=110 ms

Each V is preceded by a His The third His is obscured by the dissociated A

Site of Ablation in BBRVT

The ablation catheter is positioned at the right bundle branch during sinus rhythm, which is the site of ablation for this tachycardia. Note that the RBB spike occurs well after the His spike. In this patient, elimination of the RBB will eliminate the VT, but leaves the patient with AV conduction totally relying on the LBB. Given this patients underlying LBBB, they may likely need a pacer post ablation.

Post RBB Ablation

Successful ablation of the right bundle in a patient with BBRVT. Now that the patient can no longer have BBRVT, the RBB ablation, in conjunction with underlying LBBB has resulted in complete heart block. Notice the P waves without QRSs following. Now the patient requires a permanent pacemaker.

Post RBB Ablation

Successful ablation of the right bundle in another patient does not cause complete heart block, but I rather, leaves the patient with a permanent right bundle branch block (wide positive QRS in V1) in sinus rhythm.II Now that the the right bundle is ablated, this patient can no longer have BBRVT. This patient will probably not require a pacemaker

V1 RA

Current

Voltage

Bundle Branch Reentry and CARTO XP System Bundle branch reentry VT ablation with CARTO XP System is anatomical.
The site of the RBB potential can be demarcated for ablation.

Bundle Branch Reentry and CARTO XP System

His bundle can also be marked as to not cause inadvertent heart block. The tricuspid valve should be marked. Other sites of interest for anatomy may be delineated but are not essential.

Right Bundle Branch Location

The right bundle branch lies just distal to the His Bundle below the tricuspid valve on the superior aspect of the interventricular septum.

Site of RBB for BBRVT Ablation (with CARTO XP System) in RAO

RVOT

His

His Potential

RBB Site on Interventricular Septum just distal to the His (Successful Ablation)

RVA
RV RAO for anatomic representation of the right bundle branch location

TVA
RBB Potential

Idiopathic Left Ventricular Tachycardia Left Fascicular VT -reentry or triggered Left Ventricular Outflow Tract VT -automatic

Left Fascicular VT
Also known as verapamil sensitive VT
Left Posterior fascicular VT with a RBBB and superior axis(common) Left Anterior fascicular VT with a RBBB and right axis(uncommon) Upper septal fascicular VT with a narrow QRS and normal axis(rare)

Young patients without heart disease Posterior and anterior fascicular VT can be successfully ablated at the mid-septum guided by a diastolic Purkinje potential or at the VT exit site guided by a fused pre-systolic Purkinje potential.

Left Posterior Fascicular VT

Right bundle (positive (+) V1) superior axis (II, III, and AVF negative (-))

Left Posterior Fascicular VT

Fused pre-systolic Purkinje potential

Left Ventricular Outflow Tract VT

Three locations possible 1. Endocardial 2. Coronary cusp 3. Epicardial

Ventricular ectopy arising from the base of the left coronary cusp.

LVOT VT. CL=290 ms; RBBB morphology (+) V1. Inferior Axis (+) II, II, and AVF. Precordial leads are concordant with a positive, peaked QRS.

Limitations of EUS Technique

Many labs are unfamiliar with Unipolar pacing Requires a IVC electrode Noise on Map catheter with Unipolar pacing interferes with entrainment pacing measurements Requires significant confidence in contact of catheter with myocardium

Pace Mapping
Well established technique for Idiopathic VTs but less reliable for ischemic VTs A perfect pace match may not be achievable with scar related tachycardia 12/12 pace map represents exit site of arrhythmia Azegami et al, Pacing Clin Electrophysiol.
2002

Example of(LBB LSa) VT # 1 Pace Mapping Best PM

RAO

LV post/mid septum inferior Bipolar voltage map 1.5-.5mV

Functional Barrier During VT Only

ENTRAINMENT No QRS changes during DURING VT

pacing

PACING - NSR Trans-barrier conduction during pacing. Barrier only present in AT SOO VT; QRS changes

200ms

520ms

460ms

460ms

Entrainment Mapping
Pace from map catheter during VT at slightly faster rate than VT rate Entrainment with Concealed fusion Vs Manifest fusion Stimulus to QRS should equal local EGM to QRS during VT (within 10 msec)

= Stim-QRS = EGM-QRS

Egm-QRS

Entrainment of ventricular tachycardia (VT) at a site with a double potential is shown

Tung, S. et al. J Am Coll Cardiol 2003;42:110-115

Copyright 2003 American College of Cardiology Foundation. Restrictions may apply.

Stim to QRS During Pace Map

Provides a measure of slow conduction when Stim to QRS > 40 msec Sites with long S-QRS delays are likely in potential isthmus, infarct zone Sites with short S-QRS are likely at exit site
C.Brunckhorst et al, Circ 2004

Stim to QRS

ENTRAINMENT MAPPING

Pacing During VT
Entrain with QRS fusion (QRS change)

Entrain with Concealed Fusion (CF)

*
er L Out

*
oop

PPI = VTCL 30 ms or S QRS = EG-QRS 20 ms

No Yes

PPI = VTCL 30 ms

Is t

* mus h

r nt E

e nc a

Adjacent Bystander

S QRS / VTCL (%)

Exit

< 30%
Inner Loop

31-50% Central

51-70% Proximal

>70% Inner Loop

*
Exit

* *Adjacent bystander * * *

No Remote Bystander

Yes Outer Loop

*Remote bystanders

Targeting Late Potentials in NSR

C.Hwang, Europace 2003

Activation Map
Is useful to identify the entire circuit Can identify areas of slow conduction
Success of ablation is independent on speed of conduction through protected isthmus

Useful to identify double loops of reentry

Electrograms During VT

er L Out

o op

Is

*mus th

an tr En

ce

Exit

Inner Loop

Mid Diastolic Potentials During VT

Map potentials which precede QRS by > 50 msec Potentials must be shown to correlate during NSR to VT potentials

Mid Diastolic Potentials in VT

C.Hwang, Europace 2003

Putting It All Together

Linear lesions along border of scar to closest pace map match (exit point) Target late potentials in NSR Target mid-diastolic potentials during VT Linear lesions connecting scar to scar or scar to anatomical boundaries

Kyoko Soejima, MD et al, Circ 2002

Bundle Branch Reentrant Ventricular Tachycardia

VT From Bundle Branch Reentry

Occurs in up to 30% of VT associated with idiopathic dilated cardiomyopathy VT is usually left bundle branch block (negative QRS in V1), superior axis (negative QRS in II, III, and AVF) morphology

VT From Bundle Branch Reentry

Dependent on both bundles for reentry Baseline EKG usually will demonstrate signs of underlying conduction delay (bundle branch block) and signs of cardiac dilatation (atrial enlargement)

Goals: Ablate right bundle and abolish reentry

Baseline Sinus EKG in BBRVT

VT EKG in BBRVT

VT Due to Bundle Branch Reentry

VT Due to Bundle Branch Reentry

His Bundle

VT Due to Bundle Branch Reentry

His Bundle Right Bundle Branch Left Bundle Branch

Baseline HV in BBRVT

V-His Association in BBRVT

HRA

HV Interval=110 ms

Each V is preceded by a His The third His is obscured by the dissociated A

Site of Ablation in BBRVT

Post RBB Ablation

Post RBB Ablation

I II V1 RA

Current

Voltage