AVRT/AVNRT Warren Sonny Jackman Boston Hilton 10/6

Biosense Webster (Slides available in email/slideshare)

Saturday:
***Accessory Pathway localization and ablation: Role of the oblique course and unipolar
EGMs.***

***Parahisian RV pacing to identify VA conduction pathways***

***Anteroseptal Accessory Pathways***

***Posteroseptal Accessory Pathways***

Sunday:
***5 Atrio-Nodal connections (AV nodal pathways) and slow pathway ablation sites***`

***Anatomical definition of different forms of AVNRT and Targeting atrial end of various slow
pathways. ***

To prove an antegrade AP potential — ventricular extra stimulus!!! While pacing atrium

Mostly above the leaflet nowadays but below the leaflet historically worked.
> half of APs are left sided. On epicardial side of structurally normal heart/mitral annulus.
Atria rotate from V and cause oblique pathway.
Around ablation lesion - inflammatory line surrounding lesion, coagulation necrosis.

Endocardial RF lesion includes epicardial surface of LV

Target the atrial or ventricular end of AP from beneath the leaflet.
Pitfall - RF application could be in trabecular recess too far below the mitral annulus (tiny or no
atrial signal (far field))

Large atrial potential during sinus rhythm. tiny retrograde atrial potential
Ablation electrode beneath mitral leaflet - stable, good position but steep learning curve.

Then, transeptal approach - depends on contact force -look at curve (sine wave) not just
number. Even if number is low, if curve is good, just increase power and time.

RF lesion affects LA and LV epicardium. If too high above mitral leaflet / annulus, could just stun
the pathway and it comes back.

Small and rounded - far field

Large and sharp is closer proximity

Lower gain - sharp is sharp. High gain - even far field signal is sharp.

Localization:
Case: 24F concealed right lateral AP, 3 prior unsuccessful RF ablations. All successful but with
recurrence of AVRT. close but not directly over AP.
Oblique course across AV groove. Oblique - length along the annulus.
Oblique length of 1.8 cm = ~ 2.2 cm where you can successfully ablate (2 mm each side)
Oblique course is the most common reason for ablation failure.
Earliest atrial activation target is ALWAYS off the pathway ( most rapid conduction gives highest
signal (earliest atrial activation) which is more atrial and diffuse than true focal AP bridge.

Shortest local VA and VA Fusion are located beyond the atrial end of AP (atrial wave faster and
catches up to V conduction).

64% fractionated atrial potentials

So oblique course - traditional criteria (earliest V activation and shortest local AV interval) is
usually off. Hypothesis is based on assumption of perpendicular pathway across annulus.
Line of block causes double or split potentials
“chewed up” electro grams
Instead, ablate where AP EGM is strongest and you can get retrograde block
Where did the original criteria come from? Didn’t know about oblique course in 1970s - AP’s
cross the AV groove perpendicular to the annulus.

Traditional Localization Criteria:

Antegrade
- earliest V activation
shortest local AV interval
A-V fusion
No separate (“isolated”) AP potential.
Retrograde
earliest A activation
Shortest and Fixed VA interval
VA fusion
No separate of isolated AP potential.

Works if perpendicular but virtually all accessory pathways are oblique!

86% are oblique. Usual length is 5-30 mm (avg 10-12 mm) ALONG THE MITRAL ANNULUS.

Closely spaced electrodes - higher “resolution” of EGM

VA pacing - V potential, then Isolated AP potential (distinct EGM) then A potential

Location of V pacing matters. Either shows or hides AP potential
Antegrade pacing - pacing in one direction widened AV interval, the opposite direction, AV
interval shortens.
Pace from both sides (once side V and A fuse, useless. Other site V and A separate = good)

How to validate antegrade AP potential. Ventricular extra stimuli

Eliminate the possibilities and whatever remains is the answer - Sherlock Holmes
Maneuver during tachycardia is same as V pacing.

A , ?AP, V.
NSR - conduction is antegrade, with VES, it is retrograde.
Maneuver - ventricular extrastimulus earlier . If ?AP EGM stays same distance from A, and V
pulls in, ?AP EGM is not V. AP dissociated from A and V = AP.
If pathway, it will stay fixed to A

Reasons to validate AP
Dangerous area to ablate (av node, MCV, middle cardiac vein), near coronary artery (need
angiogram).
Prior unsuccessful ablation. Exclude double A or V potentials

PCV posterior cardiac vein

How to validate a retrograde AP potential. Atrial extra stimulus.

If AP, A will pull in and ?AP will not
If not, both may move together
Stim-A time
Local A advanced but AP unchanged proves it is not A.
AP is dissociated from local V

Overt vs concealed pathway. If concealed, conducts retrograde but never antegrade (implies
never has pre-excitation).
Break:
History - pathologist on autopsy sliced heart perpendicular so most pathways (oblique) were
missed. Airforce ECG studies showed about 2-3/1000 preexcitation. However autopsy was far
fewer. So historical initial case reports thought AP was perpendicular, most/obliques were
missed.

Jac De Bakker - best understanding of EGM review

CS catheter- distal is atrial end of AP, V insertion is proximal.

CS turns into great cardiac vein.

Demonstrate oblique course by

differential pacing
15ms arbitrary cut off for change in VA time to suggest oblique pathway.
Pacing at basal inferior RV septum or MCV

Ventricular wavefront is moving away from direction of AP insertion activation.

AP potential is unmasked by selected pacing site - critical.

Retrograde across AP. There is a delay as conduction reverses laterality direction.

The more oblique the course, the later local atrial activation will be.
Don't pace right side for left sided AP.

Ablation lesion never reaches electrode 2.

Look at unipolar EGMs to decide where to ablate successfully

Bipolar helps eliminate far field signals
Distal is + (1), - is 2
Potential difference from far field is 0. Bipole electrodes wont detect a remote potential
difference and wont generate a deflection.
Don't use bipole, just use it to find general area.
Use unipolar electro gram to target kill shot. Sharper deflection is better.
Unipole- + is mapping electrode, negative is reference electrode outside chest, sometimes
Wilson’s central terminal (60 Hz -noise, but don’t use Notch filter!) OR IVC electrode
Try not to filter a unipolar egm. 1 (high pass) -500 (low pass) Hz

Long oblique course - AP potential is observed in several contiguous leads/EGMs.

114 consecutive patients

Left free wall
Right free wall
Anteroseptal
posteroseptal

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PARA HISIAN PACING

His pacing is really RBBB pacing.

If RV parahisian pacing, V capture related to HA.

Retrograde AV nodal conduction vs retrograde AP

Stim A is surrogate for VA (but sometimes Stim V interval can vary).

3 Causes of Short Stim A
Capturing A
Capturing AP
Capturing V close to AP

Lead 1 QRS notch suggestive of ventricular capture

Narrow and no notch suggestive of His capture.

Stim A increases, HA fixed suggests AV node dependent (AVNRT) and less likely AP/AVRT.
If A pulled in with H, AVNRT

Selective vs non selective His pacing/capture (V and His vs His)

Stim A now a surrogate for HA

Activation sequence
Stim A

Para Hisian pacing based on QRS alone is why it is hard/poor. Don’t base decision of what is
captured or not on QRS morphology. NEED to note timing of His!

HH interval shortens, decremental conduction, HA increases “slightly.”

SA increased
HA “almost” fixed.

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ANTEROSEPTAL PATHWAYS
35% of all AP (but only 1/5 is really septal)
Septal space historically defined by surgical approach.
Anteroseptal and posterseptal separated His (with actual His considered anteroseptal) His or
anterior

Our definition: site recording both AP and His potentials from same 2 mm-spaced electrode.

Anterseptal divided into 4 -

tricuspid annulus sites
Right anteroseptal (Para Hisian) AP (right over His) (25%)
Right anterior paraseptal (75%)
TOGETHER are 88% of anteroseptal).
- Early, rounded delta wave in V1.

Anteroseptal:
- Look at V1 for QS
- delta wave + in I II and aVF
- V1 - V2 transition.

3. Epicardial Right anterior Paraseptal (non coronary sinus of valsalva) (8%). Cannot ablate
endocardially.

4. True Left anteroseptal (4%) - toughest

Bump ability, knock out conduction. Bump block

Usually at atrial end.
stay on ventricular side of annulus.

Sedation anesthesia can cause VA block.

Localization!:
Oblique course critical to interpretation of potentials.
Ventricular end anterior and right (70%)
Atrial posterior and left.

Basal anteroseptal RV pacing (Para Hisian pacing).

Separate V and A going one way vs opposite way.

Local VA interval changes by > 15 ms implies an oblique pathway.

Pace RA appendage or CS?

You can determine oblique from atrial extra stimulus AND ventricular ES.

Avoid AV block with RF

Keep catheter on RV side of TV
Visualize Unipolar EGM 1 with AP and no atrial potential.
May sacrifice RBundle to avoid AVN.

High midseptal pathway over compact AVN (highest risk of AVB, his is less likely to go down if
ablated).

Ablation target is AP potential, not site of earliest atrial activation!

Nothing on bipolar EGM and 2 identical on unipolar ==> far field!!

PVC and FOCAL AT. No need for GA.

All other cases, uses GA.
10-12 % of anteroseptal pathways cannot be ablated from right side tricuspid.

Left Anteroseptal:
In LV, across AoV, catheter bounces in and out. Movement can cause CHB.
Earliest retrograde atrial activation and/or AP potential at true septum (posterior to Tendon of
Today).

POSTEROSEPTAL
Huge area (6 regions)
Posterior to His bundle
Cause of most failed ablations.

Activation along CS floor and roof are often different.

Coronary sinus myocardial potentials (muscular)

Map during both:antegrade AP conduction (atrial pacing)

Retrograde AP conduction (ventricular pacing)

***Right mid septal and posteroseptal pathways (2/6) 10-15% of posteroseptals

(between His anterior and CS posterior)
Earliest antegrade V. Earliest retrograde A (difficult). Usually not in same location (oblique)

Eustachian ridge and tendon of today

Right midseptal (70% ventricular end is inferior)

Ablate under septal leaflet of TV (but can be difficult), to avoid AVB.

Pace on both sides and find the side that separates AP

SL2 catheter for right posteroseptal pathway

AP vs ASP (slow pathway)

Ablation of ASP would cause junctional automaticity and prevention of AVNRT later in life!
Just stop and pace the A faster than junctional

***Left midseptal AP - less common, rarest of posteroseptals < 1 %

During retrograde AP conduction: similar timing of “earliest” atrial activation in HBE and
proximal CS EGM.

Pushing catheter against roof of CS os can cause AVB.

A in CS roof earlier than CS floor (closer on picture)

***Left posteroseptal ~ 65% of posteroseptals

Don’t pace RV, pace from posterior coronary vein or any lateral vein/CS branch

***AP a/w CS ~ 20% of posteroseptals (~5% of all AP’s)

Small cardiac vein, PCV, GCV are veins, CS is a muscular chamber.
Anterior, superior CS os.
Pace V, add atrial extra stimulus, advance the A and thus prove not A
But ? Ventricular fragment? Pull A in even more, ?AP moves and proves its not V. Sherlock
Holmes — must be AP

Vein of Marshall
Vuscens valve

Middle cardiac vein is extension of CS myocardium

= CS-LV connection (epicardial posteroseptal AP)

3 potentials in MCV:
Retrograde CS muscle sleeve (AP) from LV
CS myocardium
LA

Of PS AP’s with prior failed ablations, ~50% are CS-LV connections!

CS-LV:
V1-V2 transition (septal)
Delta in AVF negative, isoelectric or positive ( see slide)
Delta in lead II - steep negative is almost always an epicardial PS AP (CS-LV). Very specific, less
sensitive.

196 pts
CS diverticula (muscular “bags”) ~ 20%
Fusiform or Bulbous dilatation ~ 7%
Normal anatomy ~ 74%

Ablation:
Ablate and ablate and ablate cuz pathway keeps moving down and down the more you ablate.
So ablate at the choke point

Don't be deeper in MCV than CS-LV connections.