Electrophysiological diagnosis and management of AVRT

Electrophysiological diagnosis and management of AVRT

Satyam Rajvanshi

WPW

Louis WolffJohn ParkinsonPaul Dudley White

In 1930, published article describing 11 patients who suffered from attacks of tachycardia associated with a sinus rhythm with pattern of bundle branch block with a short PR interval

Later k/a WPW syndrome!

Louis WolffJohn ParkinsonPaul Dudley White

Mechanisms of Tachyarrhythmias

Disorders of Impulse formation

Disorders of impulse conduction

Combination of both

Enhanced impulse formationAbnormal automaticity (Phase 4)Least affected by Extrastimulus testingOverdrive pacing either overdrive suppression orNo effect

Enhanced impulse formationTriggered activity (Phase 3)Least common mech of SVT eg. Digitalis induced Initiated by overdrive pacing without conduction delay or blockOverdrive pacing Acceleration

Disorders of Impulse formationAutomaticityTriggered activity EAD/DADDisorders of impulse conductionReentry Combination of both

Disorders of impulse conductionReentryPathway - Anatomic, Functional, Both

MC mechanism of SVTs

reentry

The 3 conditions for reentryAtleast 2 functional (or anatomic) distinct pathways Joining proximally and distallyForming a closed circuit of conduction

The 3 conditions for reentryUnidirectional block in 1 of the pathways

The 3 conditions for reentrySlow conduction down the unblocked pathway allowing the previously blocked pathway time to recover excitability

Sites of re-entry in SVT

AVRT: Introduction

AVRTReentrant tachycardia with an anatomically defined circuit that consists of two distinct pathways, the normal AV conduction system and an AV accessory pathway, linked by common proximal (the atria) and distal (the ventricles) tissues. Other arrhythmias can utilize the accessory pathway for conduction from the anatomic site of tachycardia origin to other regions of the heart (like AF/AFL)But AVRT is a specific reentrant tachycardia in which the accessory pathway is necessary for initiation and maintenance of the tachycardia

AVRTAccessory pathway maybeManifest/WPW

Concealed

AVRTAccessory pathway maybeManifest/WPW

Can conduct both Antegrade (A to V) & Retrograde (V to A)Abnormal ECG baselineVariable degrees of pre-excitationHigher risk with atrial fibrillation

Concealed

Retrograde (V to A) conduction onlyNormal ECG baselineNo pre-excitationAtrial fibrillation not an issue

AVRTAccessory pathway maybeManifest/WPW

Antidromic AVRT Orthodromic AVRT

Concealed

Only Orthodromic AVRT possible

20-40% SVTs in patients without pre-excitation

AVRTAccessory pathway maybeManifest/WPW

Antidromic AVRT Orthodromic AVRT

Concealed

Only Orthodromic AVRT possible

90% - Fast conducting

10% - Slow (decremental) conduction - PJRT

AV conduction in concealed APVn normal ventricular activation

AV conduction in manifest AP

Vn normal ventricular activationVp ventricular activation via AP

AV conduction in manifest AP with AV nodal delay

Vn normal ventricular activationVp ventricular activation via AP

Pre excitation syndromesPreexcitationExists when in relation to atrial events, all or some part of ventricle is activated sooner than would be expected if the impulse reached ventricle by normal AV conduction

Pre excitation syndromesOld classification various eponymsKent fibre (A-V)James fibre (Atrio-nodal)Mahaim fibre (Atrio-Fasc or Nodo-Fasc)Antidromic AVRT with LBBB + superior axisProgressive increase in the AV interval in response to atrial overdrive pacing (oppositeto the behavior of the usual AP, in which preexcitation occurs with short AV intervals)WPW syndromeLGL syndrome

Pre excitation syndromesNew classification No eponymsAtrioventricular bypass tractNodoventricular bypass tractFasciculoventricular bypass tractAV nodal bypass tract atrionodal/atriofascicular

Pre excitation syndromesNew + Old classificationAtrioventricular bypass tract: WPW syndrome

Nodoventricular bypass tract: WPW variant Fasciculoventricular bypass tract: WPW variant

Atrionodal bypass tract: LGL syndrome

WPW in Sinus Rhythm

Wolff-Parkinson-White syndrome: Preexcitation

Wolff-Parkinson-White syndrome is a form of anomalous AV conduction or ventricular pre-excitation. Ventricular pre-excitation is said to exist when conduction of a supraventricular impulses occurs via an accessory pathway which bypasses the AV node. Conduction through the accessory pathway allows premature activation of the ventricular myocardium, which is evidenced by the short PR interval and the initial slurring or notching of the QRS (the delta wave).

ECG requirements for diagnosis of WPW syndrome

Short P-R interval (< 120 ms)Normal P wave vector (to exclude junctional rhythm)Presence of a delta wave, slurring or notching of the first portionof the QRS complexQRS duration greater than 100 ms

Note that in this example, right-sided pre-excitation is followed by normal activation via the left bundle branch, producing a "fusion" complex.

Pre-excitation 12-Lead ECG

PR interval < 120 msNormal P wave vector (not ectopic atrial rhythm)Delta waveQRS duration > 100 ms

AVRT: WPW syndrome: Preexcitation 12-Lead ECG

ECG requirements for diagnosis of WPW syndrome

Short P-R interval (< 120 ms)Normal P wave vector (to exclude junctional rhythm)Presence of a delta wave, slurring or notching of the first portionof the QRS complexQRS duration greater than 100 ms

Note that in this example, right-sided pre-excitation is followed by normal activation via the left bundle branch, producing a "fusion" complex.

Orthodromic AVRTInitiated by a closely coupled APC or VPCBlocks in the accessory pathway but conducts through the AV nodeRetrograde conduction via accessory pathwayInverted P wave produced by retrograde conduction visible in the inferior ECG leads

Wolff-Parkinson-White syndrome: Initiation of AVRT

An episode of supraventricular tachycardia can be initiated by a closely coupled premature atrial complex (PAC) which blocks in the accessory pathway, but conducts through the AV node. The rapidly conducting accessory pathway is slower to recover than the AV node, but by the time ventricular depolarization is nearly complete, the bypass tract has recovered to allow retrograde conduction back to the atria. This retrograde atrial impulse is in turn conducted to the ventricles via the AV node, and the re-entrant circuit is established. The P wave produced by retrograde conduction during AV reentry tachycardia is inverted in the inferior ECG leads, since atrial depolarization begins in the lower right atrium and proceeds superiorly and leftward. Rapid retrograde conduction over the accessory pathway results in a short R-P interval, usually less than one-half of the R-R interval.

Antidromic AVRTRetrograde conduction via AV nodeAntegrade via AP

Orthodromic AVRT: 12-Lead ECGVentricular rate typically 150 250/min (or greater) beats per minute, regularNarrowQRS complexes (in the absence of underlying IVCD)Inverted P waves with an RP interval usually 50%the tachycardia RR interval (RP > PR)Constant RP interval regardless of the tachycardia cycle length

AP LocationAnywhere along the muscular portion of the posterior and lateral aspects of the mitral and tricuspid annuli.

Schematic from base of heartFrom LAO view

Wolff-Parkinson-White syndrome Extra-nodal AV conduction pathways

Atrioventricular bypass tracts, or accessory pathways, can be found anywhere along the muscular portion of the posterior and lateral aspects of the mitral and tricuspid annuli. They can be classified by their anatomic location as either

right-sided,left-sided, posteroseptal, or anteroseptal.

Patients with Wolff-Parkinson-White syndrome have an accessory pathway that can conduct in both an anterograde or retrograde direction. As we will see on the next page, anterograde conduction via the accessory pathway during sinus rhythm bypasses the AV node, pre-exciting the ventricle and producing the characteristic delta wave.

Patients with an accessory pathway capable only of retrograde conduction are said to have a concealed bypass tract, because a delta wave is not seen during sinus rhythm.

AP LocationNone of the various algorithm is perfectSimplest algorithm, Fitzpatrick -

EP Diagnosis of AVRT

The 3 characteristics of reentryInitiated by timed extrastimulus more effectively than rapid pacingProgrammed stimulation can also terminate Tachy

The 3 characteristics of reentryNo direct relation of pacing cycle length to the tachy cycle length

The 3 characteristics of reentryExtrastimulus can reset or entrain the Tachycardia in presence of fusion

6 tenets of SVT evaluation

1Mode of initiationRelation ofBasic drive cycle lengthES coupling intervalOnset of tachyTachy cycle length

Differentiates triggered activity from reentry

2Atrial activation sequenceP-QRS relation

3Effect of BBB during TachySpontaneous or induced BBBOn cycle lengthV-A conduction time

4Requirement of atria, HB, Ventricle in initation and maintenance of tachyEffect of AV dissociation on tachy

5Effect of atrial or ventricular stimulation during tachy

6Effect of drugs or physiological maneuvers during Tachy

AVRT: Baseline observation during NSRH-V < 35 ms, may be negativeHis potential can be buried in the local ventricular EGMSite of earliest ventricular activation is near the ventricular insertion site of the AP (i.e., near the tricuspid annulus or mitral annulus at the base of the heart)Slowing of conduction in the AVN by carotid sinus massage, AVN blockers, or rapid atrial pacing unmasks and increases the degree of preexcitation, because these maneuvers do not affect the conduction over the AP.

HV -11 ms at AES 600 ms HV -65 ms at AES 440 ms

HV -93 ms at AES 350 msLess preexcitation on sinus beat

AES during NSRIn the presence of a manifest AV-AP, atrial stimulation from any atrial site can help unmask preexcitation if it is not manifest during NSR caused by fast AVN conduction. Incremental rate atrial pacing and progressively premature AES produce decremental conduction over the AVN (but not over the AP), increasing the degree of preexcitation and shortening the HV interval, until the His potential is inscribed within the QRS. The His potential is still activated anterogradely over the AVN until anterograde block in the AVN occurs; the QRS then becomes fully preexcited, and the His potential becomes retrogradely activatedAtrial stimulation close to or at the AV AP insertion site results in maximal preexcitation and the shortest P-delta Interval

Retrograde His activation and echo beat

AES during NSRThe failure of atrial stimulation to increase the amount of preexcitation can be caused by markedly enhanced AVN conductionpresence of another AV-APpacing-induced block in the AV AP because of a long ERP of the AP (longer than that of the AVN)total preexcitation already present at the basal state caused by prolonged or absent AVN-HPS conduction, and/or decremental conduction in the AP

VES during NSRIndicators of the presence of a retrogradely conducting AV APVES resulting in retrograde VA conduction eccentric atrial activation sequenceVES delivered when the HB is refractory that results in atrial activationHowever, if a VES delivered when the HB is refractory does not result in atrial activation, this does not necessarily exclude the presence of a retrogradely conducting AP, because such a VES can be associated with retrograde block in the AP itself, or presence of unidirectional (anterograde-only) APs

VES during NSRIn the presence of a retrogradely conducting AV BT (whether manifest or concealed), VES during NSR can result in VA conduction over the BT, AVN, both, or neitherConduction over the AP alone is the most common pattern at short pacing CLs or short VES coupling intervals. In this case, the VA conduction time is constant over a wide range of pacing CLs and VES coupling intervals, (in the absence of intraventricular conduction abnormalities or additional Aps)On the other hand, retrograde conduction over the BT and HPS-AVN is common when RV pacing is performed in the presence of a left-sided BT at long pacing CLs or long VES coupling intervals

A- Retrograde atrial activation by both AVN and APB- retrograde atrial activation by AP alone Eccentric activation

Type of eccentric atrial activation on location of APLeft lateral AP

Right lateral AP A in HRA before CS

Posterosepatal AP A in PCS before HBE

AVRT induction: Orthodromic AVRTInitiation of orthodromic AVRT with an AES requires Anterograde block in the AV-BTAnterograde conduction over the AVN-HPSSlow conduction over the AVN-HPS, with adequate delay to allow for the recovery of the atrium and AV BT Subsequent retrograde conduction over the BTThe reason this occurs is because, whereas the BT conducts more rapidly than the AVN, it has a longer ERP, so the early atrial impulse blocks anterogradely in the BT but conducts over the AVN. The site of AV delay is less important; it is most commonly in the AVN, but it can occur also in the HB, bundle branches, or ventricular myocardium.BBB ipsilateral to the AV BT provides an additional AV delay that can facilitate tachycardia initiation.Induction of orthodromic AVRT is easier with AES near the AV BT insertion site; the closer the stimulation site to the BT, the easier it is to encroach on the refractory period of the BT and achieve block

If SVT induction fails by AESuse of multiple AESsRapid atrial pacingpacing closer to the BT would achieve block in the BT and produce adequate AV delay

Orthodromic AVRT in patients with concealed BTs is identical to that in patients with WPW. The only difference is that in patients with concealed BTs anterograde block in the BT is already present. Because the AV BT does not conduct anterogradely, the only condition needed to induce orthodromic AVRT is adequate AV delay Therefore, orthodromic AVRT initiation requires less premature coupling intervals of the AESs in patients with concealed BTs than in patients with WPW.

AVRT is more easily induced by VES

Orthodromic AVRT: Tachycardia features

Atrial activation sequence first activation closest to AP insertion siteFast conduction in AP - Short RP interval (50-120 ms) but longer than AVNRTBBB much more common in AVRT (than AVNRT or AT) 90% of sustained SVTs with BBB AVRT

CSM can terminate orthodromic AVRT by gradual slowing and then block in the AVN. Adenosine, digoxin, CCB, and BB terminate orthodromic AVRT by block in the AVN - therefore, SVT terminates with a P wave not followed by a QRS

Antidromic AVRT: Tachycardia features

RP > PR interval PR short and fixedRest features similar to Orthodromic AVRT

AES/VES during tachycardiaClose coupled AES/VES affect AVRTEntrainmentFusionTerminationAbility of AES/VES to affect the SVT depends on the distance between site of stimulation to the AP and coupling interval

Exclusion of AVNRTPPI post pacing interval

Location of APPacing from Multiple Atrial Sites. The closer the pacing site to the BT atrial insertion, the more rapidly the impulse will reach the BT relative to the AVN and thus the greater the degree of preexcitation and the shorter the P-delta interval.Effects of Bundle Branch Block During Orthodromic AVRTEarliest atrial and ventricular activation sitesDirect recording of BT potential

Ablation

Criteria of Successful Ablation Sites during Anterograde Activation Mapping

Additional criteria during retrograde Activation Mapping

AVRT: Catheter Ablation Of Accessory PathwayRadio frequency ablation of the accessory pathway is often indicated in patients with WPW who are at risk of sudden death due to atrial fibrillation with a rapid ventricular response via the bypass tract.

Note the disappearance of the pre-excitation delta wave in the QRS with catheter ablation.

Wolff-Parkinson-White syndrome: Ablation of Accessory Pathway

Radio frequency ablation of the accessory pathway is often indicated in patients with WPW who are at risk of sudden death due to atrial fibrillation with a rapid ventricular response via the bypass tract.

Note the disappearance of the preexcitation delta wave in the QRS with catheter ablation.

AVRT: Catheter Ablation

Retrograde ablation of left side AP, RAOAblation of right side AP

SDSD73

Precise location of the accessory pathway is determined by the rove catheter. Retrograde conduction over the AP is seen as a small spike between the V and A waves. These "Kent potentials" are so named because of the original denomination of accessory pathways as "Kent bundles," after the investigator Stanley Kent, who first proposed the existence of accessory AV connections.

AVRT: Catheter Ablation - Location of AP

AV Reentry Tachycardia: Mapping of Kent Potentials

Precise location of the accessory pathway is determined by a mapping catheter. Retrograde conduction over the AP is seen as a small spike between the V and A waves. These "Kent potentials" are so named because of the original denomination of accessory pathways as "Kent bundles," after the investigator Stanley Kent, who first proposed the existence of accessory AV connections.

Ablation techniqueIf preexcitation present (Manifest AP) ablation performed during NSR or, preferably, atrial pacing allows detection of delta waveFor concealed AP Ablation during ventricular pacing, allows for detection of an eccentric atrial activation sequence. RF energy delivery during AVRT avoided because of potential catheter dislodgment from its critical position on abrupt tachycardia termination can cause transient loss of conduction in AP for a variable period of time without resulting in permanent damage to the APFor incessant AVRT, energy may be delivered during ventricular pacing entraining the tachycardia

Ablation technique4 mm tip ablation catheter sufficient Power 50 WTemperature 60 degreeAP functional loss at 50 degreesAP permanent loss at 60 degrees do not stop till 55-60 degrees is achieved by good contact (larger tip catheter are rarely needed)

Ablation techniqueLoss of BT conduction is expected within 1 to 6 seconds of RF application (once the target temperature and power delivery have been reached) for most successful lesions.If no effect is seen after 15 seconds of RF delivery, energy delivery should be discontinued because it is unlikely to be beneficial, and mapping criteria and catheter contact should be reexamined. If BT conduction is eliminated during the application, RF delivery should be continued for up to 60 seconds.

Ablation techniqueIf BT function is not eliminated at a site with apparent favorable electrographic features, catheter contact with the tissue may be inadequate. Adequacy of catheter contact can be verified by evaluating the electrode temperature, catheter stability on fluoroscopy, electrogram stability, and ST elevation on the unipolar electrogram. If electrode temperature is consistently more than 50C with more than 25 W energy delivered to the tissue during the RF application - good catheter contactIf electrode temperature is lower than 20C with more than 25 W energy bad catheter contactIf electrode temperature reaches more than 50C but with very low power (less than 10 W) - coagulum at the catheter tip

AVRT: Catheter Ablation

Wolff-Parkinson-White syndrome: Ablation of Accessory Pathway

Radio frequency ablation of the accessory pathway is often indicated in patients with WPW who are at risk of sudden death due to atrial fibrillation with a rapid ventricular response via the bypass tract.

Note the disappearance of the preexcitation delta wave in the QRS with catheter ablation.

Endpoints of ablation

Successful ablationConfirmation of complete loss of BT function, and not just noninducibility of tachycardias, is essential.

Confirmation of complete loss of anterograde BT function using AES and atrial pacing no preexcitationMarked prolongation of the local AV interval at the ablation site.

Confirmation of complete loss of retrograde BT function using VES and ventricular pacing - concentric and decremental retrograde atrial activation normal VA conduction over the AVNMarked prolongation of the local VA interval at the ablation site.

outcome

RF ablation is a highly effective and curative treatment for AVRT (more than 90%)Initially successful RF ablation is persistent and late recurrence of BT conduction after ablation is rare (4%)

Short runs of palpitations are frequent post RFA, usually caused by isolated or short runs of PACs or PVCs and not by recurrence of BT conduction, and can be easily managed with symptomatic treatment without further investigation.

Recurrence of AP-mediated tachycardia is usually observed during the first month after ablationLater symptoms (palpitations appearing more than 3 months after the ablation) are highly suggestive of SVTs not related to the ablated AP 10 to 30% patients with AVRT have multiple pathways for tachycardias

Repeat procedures 2-4% Serious complication (e.g., cardiac tamponade, AV block, coronary artery injury, retroperitoneal hemorrhage, stroke)