PRE-EXCITATION SYNDROMES

Abnet October 30,2017

Harrison’s 19th ed.
UpToDate 21.6
INTRODUCTION
 Patients with a preexcitation syndrome have an
additional pathway, known as an accessory pathway
(AP), which directly connects the atria and
ventricles, thereby allowing electrical activity to
bypass the AV node

 Tissue in the accessory pathways, which are

congenital in origin and result from failure of
resorption of the myocardial syncytium at the
annulus fibrosis of the atrioventricular valves during
fetal development
 Typicallyconducts electrical impulses more quickly than
the AV node, resulting in the shorter PR interval seen on
the surface ECG
INTRODUCTION
 In the absence of an AP, the sinus impulse
normally activates the ventricles via the AV node
and His-Purkinje system, resulting in a PR
interval of 120–200 ms.

 When an antegradely conducting AP is present,

the sinus impulse bypasses the AV node and can
activate the ventricles rapidly, resulting in
ventricular preexcitation
CHARACTERSTICS OF APS
 60 to 75 percent of APs: Capable of bidirectional
conduction (anterograde and retrograde)

 17 to 37 percent: Capable of only retrograde

conduction (VA)
 When accessory pathways conduct exclusively in the
retrograde direction: Called “Concealed" APs

 Concealed APs: do not generate a delta wave and

the WPW pattern on the surface ECG but are
still capable of supporting reentrant tachycardia
(discussed in detail later)
CHARACTERSTICS OF APS
 5 to 27 percent: An AP capable of only
anterograde conduction
 In such cases, it can form the antegrade arm of an
antidromic AVRT circuit.

 The mechanism responsible for unidirectional

conduction along an accessory pathway
(anterograde only or retrograde only) remains
undetermined
WPW: EKG DURING SINUS RYTHM
 The resulting PR interval is shorter than
anticipated.

 In addition, because the initial ventricular

activation is due to muscle-to-muscle conduction,
as opposed to rapid spread of activation via the
His-Purkinje system, the initial portion of the
QRS complex is slurred, creating the
characteristic "delta wave."
WPW: EKG DURING SINUS RYTHM
 The remaining portion of the QRS complex in
sinus rhythm is created by a fusion of the
ventricular activation wavefront originating from
the Purkinje network and the continued spread
of activation from the site of insertion of the
AP

 Evidence of ventricular preexcitation includes

evidence in sinus rhythm of a short PR interval
and a delta wave.
The delta wave occurs because a portion of the
ventricles are activated instantaneously via the AP.
The remainder of the QRS is normal, because it is
activated via the AV node and His-Purkinje system.
When an AP conducts only in a retrograde
direction (from ventricle to atrium), there is no
ventricular preexcitation, resulting in a normal-
appearing ECG in sinus rhythm. This is referredto
as a “concealed” pathway, because it is only
apparent when there is tachycardia. Occasionally, a
pathway that conducts anterogradely may appear
concealed if intrinsic AV nodal conduction is rapid
or if the AP is located far from the sinus node.
WPW PATTERN VERSUS WPW
SYNDROME 
 Two terms, distinguished by the presence or
absence of arrhythmias, have been used to
describe patients with accessory pathways (AP):
 The Wolff-Parkinson-White (WPW) pattern is
applied to the patient with preexcitation manifest on
an ECG in the absence of symptomatic arrhythmias.

 The Wolff-Parkinson-White (WPW) syndrome is

applied to the patient with both preexcitation
manifest on an ECG and symptomatic arrhythmias
involving the accessory pathway
LOCATIONS OF APS
 APs may be located anywhere along the AV ring (groove) or in
the septum.
 The most frequent locations are
 Left lateral (50 percent),
 Posteroseptal (30 percent),
 Right anteroseptal (10 percent), and
 Right lateral (10 percent) .Furthermore, up to 13 percent of
individuals with preexcitation have more than one accessory pathwa
 APs typically insert from the atrium into the adjacent
ventricular myocardium.

 However, occasionally pathways, particularly those originating

from the right atrium, can have a ventricular insertion at a
site distant from the AV groove in the fascicles.
LOCATIONS OF APS
 These pathways conduct more slowly and are
referred to as atriofascicular accessory
pathways.
 Atriofascicular
APs are unique in their tendency to
demonstrate decremental antegrade conduction

 Other accessory pathway connections from the

AV node to the fascicles may exist.
 These pathways are referred to as Mahaim fibers
and typically manifest a normal PR interval with a
delta wave.
 Proposed or
Old terminology commonly used Anatomic connections
terminology
Kent bundle Accessory Atrium to ventricle
(WPW Syndrome) atrioventricular (AV)
connection or AV
bypass tract
James fiber Atrionodal bypass tract Atrium to low AV node
(Lown-Ganong- Atriofascicular bypass Atrium to bundle of His
Levine syndrome) tract

Atriofascicular bypass Atrium to bundle branch

Mahaim fiber tract
Nodofascicular bypass AV node to bundle branch
tract
Nodoventricular bypass AV node to ventricular
tract tissue
Fasciculoventricular Bundle branch to
bypass tract ventricular tissue
ASSOCIATED CARDIAC
ABNORMALITIES
 Most patients with atrioventricular accessory
pathways do not have coexisting structural
cardiac abnormalities
 Associated congenital heart disease, when
present, is more likely to be right-sided than
left-sided in location
 Ebstein's anomaly: the congenital lesion most
strongly associated with WPW syndrome.
 As many as 10 to 20 percent of such patients have
one or more accessory pathway
 The majority of these are located in the right free
wall and right posteroseptal spaces
ASSOCIATED CARDIAC
ABNORMALITIES
 An association between mitral valve prolapse and
left-sided bypass tracts has also been reported.

 However, this association may simply reflect the

random coexistence of two relatively common
conditions

 In addition, a familial form of WPW is

associated with hypertrophic cardiomyopathy
PREVALENCE OF WPW
 WPW pattern: 0.13 to 0.25 percent in the general
population
 The prevalence appears higher (up to 0.55 percent) among
first-degree relatives of persons with WPW pattern,
suggesting a familial component.

 WPW pattern between 10 and 100 times more common

than WPW syndrome.

 Familial WPW  — Among patients with the WPW

syndrome, 3.4 percent have first degree-relatives
with a preexcitation syndrome
A familial form of WPW has infrequently been reported
and is usually inherited as an autosomal dominant trait
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Tachycardias associated with the WPW
syndrome can be classified into
 Those in which the accessory pathway is necessary
for initiation and maintenance of the tachycardia and

 Those in which the bypass tract acts as a

"bystander", providing a route of conduction from
the anatomic site of tachycardia origin to other
regions of the heart
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Tachycardias requiring an AP for initiation and
maintenance
 AVRT is a reentrant 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.

 If sufficient differences in conduction time and

refractoriness exist between the normal conduction
system and the bypass tract, a properly timed
premature impulse of atrial, junctional, or ventricular
origin can initiate reentry.
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Tachycardias requiring an AP for initiation and
maintenance
 The two major forms of this type of arrhythmia in
the WPW syndrome are orthodromic and antidromic
AVRT.

 The width of the QRS complex can usually

distinguish between these paroxysmal arrhythmias.
ARRHYTHMIAS ASSOCIATED WITH
WPW
 AVRT
 Importantly, these tachycardias associated with APs
involve a large macroreentrant circuit that includes
the ventricles.

 Thus, identifying these arrhythmias as

"supraventricular" is actually a misnomer, and they
deserve separate consideration.
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Orthodromic AVRT
 Ventricular activation occurs via the AV node and the
His-Purkinje system.

 Conduction then returns or reenters the atria via

retrograde conduction over the AP.

 The reentrant circuit develops because of the

inhomogeneity in conduction and refractoriness in
the AP and the normal AV node.
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Orthodromic AVRT ctd
 Characteristically,the AP has more rapid conduction
but a longer refractory period than that of the AV
node.
 Typical APs do not show evidence of antegrade decremental
conduction.
 An APC can block in the AP and conduct sufficiently
slowly or with decrement via the AV node to allow for
retrograde recovery of activation of the AP and, in
turn, of the atria

 Thisretrograde activation of the atria via the AP is

referred to as an echo beat.
 If the pattern repeats itself, a tachycardia develops
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Orthodromic AVRT ctd
 The antegrade limb (ie, the pathway that conducts
the impulse to the ventricle) is the AV node/His-
Purkinje system

 In this setting, the delta wave seen during sinus

rhythm is lost since antegrade conduction is not via
the accessory pathway (ie, the ventricle is not
preexcited)
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Orthodromic AVRT ctd
 The ECG during orthodromic AVRT typically shows
the following:
 Ventricular rate ranging from 150 to 250 (or greater)
beats per minute and usually regular
 Narrow QRS complexes (in the absence of underlying

conduction system disease or in the absence of aberrancy)

 Inverted P waves with an RP interval that is usually less

than one-half the tachycardia RR interval

 Constant RP interval regardless of the tachycardia cycle

length
 Beat-to-beat oscillation in QRS amplitude (QRS alternans)
sometimes occurs during orthodromic AVRT and is most
commonly seen when the rate is very rapid . The mechanism
for QRS alternans is not clear but may in part result from
oscillations in the relative refractory period of the His-
Purkinje system .
 Ischemic-appearing ST segment depression also can occur
during orthodromic AVRT, even in young individuals who are
unlikely to have coronary artery disease . Several factors may
contribute to the ST segment depression in these
arrhythmias, including changes in autonomic nervous system
tone, intraventricular conduction disturbances, a longer
ventriculoatrial interval, and a retrograde P wave of longer
duration that overlaps into the ST segment . The location of
the ST segment changes may vary with the location of the
accessory pathway
 P waves will generally appear within the ST-T wave
segment, with an intermediate RP interval. Though
often difficult to distinguish from AVNRT the
difference in the RP interval (intermediate vs.
short) may be helpful in making the diagnosis by
ECG. Additionally, STsegment depression in either
the inferior or precordial leads resembling that of
cardiac ischemia may be present in OAVRT and
may be a clue to the AP’s location
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Antidromic AVRT
 Uncommonly, the reentrant circuit can be reversed
so that the impulse reaches the ventricle via the AP
and conducts retrogradely through to the atria via
the His-Purkinje system and the AV node;
 This is referred to as antidromic AV reentry and/or
preexcitation macroreentry, with the entire activation of
the ventricle originating from the site of insertion of the
AP.

 Although it is uncommon, it is important to recognize

antidromic SVT.
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Antidromic AVRT
 The ECG pattern during the tachycardia mimics VT
originating from the site of ventricular insertion of
the AP.

 The presence of manifest preexcitation in sinus

rhythm provides a valuable clue to the diagnosis.
 Antidromic AVRT
 The ECG during antidromic AVRT typically shows the
following:
 Ventricular rate ranging from 150 to 250 (or greater)
beats per minute and usually regular
 Wide QRS complexes which are fully preexcited

 Inverted P waves with an RP interval that is usually more

than one-half the tachycardia RR interval and a short PR

interval
 Constant RP interval regardless of the tachycardia cycle

length
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Tachycardias not requiring an accessory
pathway for initiation and maintenance
 These include
 Atrial tachyarrhythmias,
 Junctional tachycardias including AVNRT,

 Ventricular tachycardia and ventricular fibrillation

 In these settings, the accessory pathway may serve

as a route for ventricular or atrial activation but is
generally not involved in the initiation of the
arrhythmia and is not required for perpetuation of
the arrhythmia.
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Tachycardias not requiring an accessory
pathway for initiation and maintenance
 Tachycardias that involve accessory pathways (APs)
between atria and ventricles commonly manifest a
normal QRS complex with a short or long RP interval.

 They must be considered in the differential

diagnosis of other narrow-complex tachycardias.
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Atrial Fibrillation
 Among these, the most common and potentially more
serious arrhythmia is rapidly conducting Atrial
Fibrillation

 Nearly 50% of patients with evidence of APs are

predisposed to episodes of AF.

 The QRS pattern during AF in patients with

manifest preexcitation can appear quite bizarre and
change on a beat-to-beat basis due to the variability
in the degree of fusion from activation over the AV
node
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Atrial Fibrillation
 ECG: An irregularly irregular rhythm with QRS
morphology changes from beat to beat and which
may be associated with rapid AV transmission
 A sustained ventricular rate greater than 180 to 200 beats
per minute can create "pseudoregularized" RR intervals
when the ECG is recorded at standard speed (25 mm per
second).

 When atrial impulses are transmitted along the accessory

pathway in AF, ventricular rates may exceed 300 beats per
minute and can degenerate into ventricular fibrillation.
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Atrial Fibrillation
 The QRS morphology and rate of impulse conduction
during AF along the accessory pathway is dependent
upon several factors, including:
1. The shorter the refractory period of the AP, the more
rapid is antegrade impulse conduction and, because of
more preexcitation, the QRS complexes are wider.
 Patients with very short refractory periods and rapid AF

represent the group at greatest risk for degeneration to

ventricular fibrillation
2. The degree to which the AV node/His-Purkinje system
competes with the bypass tract for ventricular activation.

3. Retrograde activation of the AP.

ARRHYTHMIAS ASSOCIATED WITH
WPW
 Atrial Fibrillation
 AF is often preceded by AVRT in individuals with
WPW, with one report suggesting that as many as 35
percent of episodes of AF were preceded by AVRT

 However, the mechanisms by which AVRT

precipitates AF are not well understood
 But increased stretching due to increased atrial pressure
and conduction disturbances in atrial myocardium due to
reduced refractoriness could play a role.
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Atrial flutter
 Atrial flutter is due to a reentrant circuit within the
right atrium and therefore exists independently of
the accessory pathway.

 Atrialflutter can, like atrial fibrillation, conduct

antegrade via an accessory pathway causing a
preexcited tachycardia
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Atrial flutter
 Depending upon the various refractory periods of
the normal and pathologic AV accessory pathways,
atrial flutter potentially could conduct 1:1 to the
ventricles during a preexcited tachycardia, making
the arrhythmia difficult to distinguish from
ventricular tachycardia.

 When atrial flutter is transmitted antegrade along

the accessory pathway, ventricular rates may exceed
300 beats per minute and can degenerate into
ventricular fibrillation.
ARRHYTHMIAS ASSOCIATED WITH
WPW
 Atrioventricular nodal reentrant tachycardia
 AVNRT (also called junctional reciprocating
tachycardia) can use the bystander accessory
pathway to transmit impulses between the atrium to
the ventricle

 When AVNRT occurs in the WPW syndrome, the

arrhythmia cannot be distinguished from either
antidromic or orthodromic AVRT without
electrophysiologic studies
CONCEALED APS
 In ~50% of patients with APs, there is no
antegrade conduction over the AP
 However, retrograde conduction is preserved.

 As a result, the AP is not manifest in sinus

rhythm and is manifest only during the sustained
tachycardia.
 The presence of a concealed AP is suggested by
the timing and pattern of atrial activation during
the tachycardia: the P wave typically follows
ventricular activation with a short RP wave
interval
CONCEALED APS
 Because many APs connect the left ventricle to
the left atrium, the pattern of atrial activation
during the tachycardia frequently produces
negative P waves in leads I and aVL.

 The tachycardia circuit and therefore its ECG

manifestation during orthodromic tachycardia
are identical both in patients with overt
preexcitation in sinus rhythm and in those with
concealed APs.
CONCEALED APS
 Patients with concealed APs, although prone to
episodes of AF, are not at risk for developing a
rapid ventricular response to the AF.

 Occasionally, APs conduct extremely slowly in a

retrograde fashion, resulting in longer
retrograde conduction and the development of a
long RP interval during the tachycardia (long RP
tachycardia).
CONCEALED APS
 Because of the presence of this dramatically
slowed conduction, additional conduction slowing
created by premature atrial complexes is not
required for tachycardia to ensue.

 These patients are more prone to frequent

episodes of tachycardia and can present with
"incessant" tachycardias and tachycardia-
induced LV cardiomyopathy
CONCEALED APS
 The correct diagnosis of a long RP tachycardia
may be suggested by the pattern of initiation
and the P-wave morphology.

 Frequently, however, an electrophysiologic

evaluation is required to establish the diagnosis
EVALUATION- ECG
 The classic electrocardiographic pattern of
preexcitation in sinus rhythm in persons with
either the WPW pattern or WPW syndrome has
two major features:
 The PR interval is short (less than 0.12 seconds) due
to rapid AV conduction through the accessory
pathway and bypass of the atrioventricular node.

 Slurring of the initial part of the QRS- Delta wave

EVALUATION- ECG
 The QRS complex consists of fusion between
early and direct ventricular myocardial activation
caused by preexcitation and the later ventricular
activation resulting from transmission through
the AV node and the infranodal conduction
system to the ventricles.

 While beginning earlier than expected, the initial

part of ventricular activation is slowed, and the
upstroke of the QRS complex is slurred because
of slow muscle fiber-to-muscle fiber conduction.
 This is termed a delta wave .
EVALUATION- ECG
 The more rapid the conduction along the
accessory pathway, the greater the amount of
myocardium depolarized via the accessory
pathway, resulting in a more prominent or wider
delta wave, and increasing prolongation of the
QRS complex.
EVALUATION- ELECTROPHYSIOLOGIC
TESTING (EPS)
 Indications for EPS for WPW: still evolving

 In most instances, EPS is not required to make

the diagnosis of WPW pattern or syndrome, but
EPS is sometimes combined with mapping and
transcatheter ablation of the accessory pathway
for both diagnostic and therapeutic purposes
during the same session.
EVALUATION- ELECTROPHYSIOLOGIC
TESTING (EPS)
 We proceed with EPS in situations when the
 Diagnosis is uncertain based on the surface ECG,
 For risk stratification purposes when a higher risk
would alter the approach to therapy, and
 As part of a therapeutic catheter ablation procedure.

 Thus, for symptomatic patients with a history of

one or more tachycardia events and manifest
preexcitation on their ECG, EPS with ablation is
now routinely offered early in the course of
management as a potentially definitive treatment
for the condition.
EVALUATION- ELECTROPHYSIOLOGIC
TESTING (EPS)
 The more difficult decision involves otherwise
healthy patients with preexcitation on their ECG
but no symptoms (ie, WPW pattern) and no
cardiac comorbidities.

 In such cases, the principle reasons for EPS are:

 To confirm the diagnosis if doubt exists
 To determine if the accessory pathway is capable of
supporting reentrant tachycardia.
 To measure the conduction characteristics of the
accessory pathway in an effort to estimate the
patient's risk for rapid conduction if an episode of
atrial fibrillation were to develop in the future.
EVALUATION- ELECTROPHYSIOLOGIC
TESTING (EPS)
 In essence, EPS is used in asymptomatic patients with the
WPW pattern as a risk-stratification tool, with ablation added
if that risk is deemed to be high

 Before proceeding with EPS for this purpose, it may be

possible to estimate risk in some cases by less invasive means.

 The observation of an abrupt and unambiguous loss of

preexcitation at faster sinus rates on ECG, Holter monitor, or
exercise testing may be a sufficient sign that the accessory
pathway has limited anterograde conduction potential and is
unlikely to result in life-threatening ventricular rates during
atrial fibrillation.
 Expert consensus is that these "low-risk" patients can usually be
followed without invasive testing as long as they remain asymptomatic
EVALUATION- ELECTROPHYSIOLOGIC
TESTING (EPS)
 If preexcitation persists at maximum heart
rates during exercise testing, it does not
necessarily mean that the patient is "high-risk",
but rather that the risk cannot be determined
by noninvasive means.

 A decision to proceed to EPS in these

indeterminate cases for better resolution of
accessory pathway profile must be made on a
case-by-case basis with careful discussion
between clinician and patient
RISK STRATIFICATION
 Patients who initially present with the WPW pattern
on surface electrocardiogram (ECG) but without a
symptomatic arrhythmia represent a significant
clinical challenge with regard to risk stratification
and management.

 The majority of such asymptomatic WPW patients,

who are often young and otherwise healthy, will
remain asymptomatic

 However, the reported rates of symptomatic

arrhythmia development have been as high as 20%
over three years
RISK STRATIFICATION
 One approach to asymptomatic patients with
WPW syndrome is risk stratification using
 Noninvasive tests and/or 
 An electrophysiologic (EP) study to identify those
patients at greatest risk
RISK STRATIFICATION
 The mechanism of sudden cardiac death (SCD) in
patients with WPW syndrome is ventricular
fibrillation (VF)
 Generally occurs during an episode of atrial
fibrillation in which there is frequent conduction to
the ventricle, leading to an excessively rapid
ventricular response that degenerates into VF.

 Identifying asymptomatic patients at the

greatest risk for VF would provide a rationale
for more aggressive therapy (eg, catheter
ablation).
RISK STRATIFICATION
 There is conflicting evidence as to which
findings predict the development of
symptoms and/or SCD.

 Some of the findings that have been suggested

to predict a higher likelihood of symptoms
include:
 Younger age
 Male gender
 Inducible AVRT or AF during EP study
 Multiple accessory pathways
 Short refractory period of the accessory pathway
RISK STRATIFICATION
 The refractory period refers to the amount of
time required after one conducted impulse for
the accessory pathway (or any cardiac tissue) to
"reset" and be able to conduct a subsequent
impulse

 This characteristic often defines how frequently

an accessory pathway can conduct to the
ventricle
RISK STRATIFICATION
 Risk stratification of asymptomatic patients with
the WPW pattern can be performed noninvasively
or via invasive electrophysiology (EP) study.
 Noninvasive evaluation
 Although the refractory period of an accessory pathway
is usually measured during an EP study, patients with an
accessory pathway that has a long refractory period can
often be identified noninvasively.
 Intermittent loss of preexcitation (as detected by loss
of delta wave on ECG) suggests that the accessory
pathway has a long refractory period and will not be
able to conduct frequently enough during AF to produce
ventricular fibrillation.
RISK STRATIFICATION
 Intermittent preexcitation or loss of preexcitation
may be seen in the following settings:
 Resting ECG
 At increased heart rates during exercise
 Following intravenous administration of a sodium
channel blocker, such as procainamide 

 One suggested approach in asymptomatic patients

is to perform noninvasive studies (eg, exercise
testing or procainamide challenge) to identify
those at low risk who would require no further
evaluation or treatment
RISK STRATIFICATION
 Patients without these low-risk findings,
particularly those under age 35 to 40, could then
consider further risk stratification and
treatment with invasive EP study.

 Decisions to proceed would be based upon the

patient's values, occupation, and activity level.
RISK STRATIFICATION
 Invasive EP study
 An alternative approach to noninvasive risk
stratification is to proceed directly to EP study as
an initial means of risk stratification in all patients
with an asymptomatic WPW ECG pattern
RISK STRATIFICATION
 In summary, initial risk-stratification with EP
study successfully identified those with a higher
likelihood of developing symptoms, and treatment
of these high risk patients with ablation reduced
arrhythmic events

 However, life-threatening arrhythmias were rare

in the absence of ablation and serious
complications developed in 2 percent of patients
undergoing risk stratification
 Thus, it remains unknown whether initial risk
stratification with EP study produces a net reduction
in morbidity or mortality
TREATMENT
 Acute treatment of AP-mediated
macroreentrant orthodromic tachycardias is
similar to that for AV nodal reentry and is
directed at altering conduction in the AV node

 Vagal stimulation with the Valsalva maneuver and

carotid sinus pressure may create sufficient AV
nodal slowing to terminate the AVRT.
TREATMENT
 Intravenous administration of adenosine, 6–12
mg, is first-line pharmacologic therapy; IV, the
calcium channel blockers verapamil and diltiazem
or beta blockers may also be effective

 Chronic oral administration of beta blockers

and/or verapamil or diltiazem may be used to
prevent recurrent supraventricular reentrant
tachycardias associated with APs.
 ANTIDROMIC AV REENTRANT TACHYCARDIA  — An
antidromic AV reentrant tachycardia (AAVRT), in which
the antegrade limb uses the accessory pathway, presents
with a wide QRS complex. Prior to therapy, it must be
distinguished from other causes of a wide QRS complex
tachycardia, primarily ventricular tachycardia.
 Acute termination  — The intravenous drug of choice for
acute treatment to terminate AAVRT is procainamide .
Even if it does not result in tachycardia termination,
intravenous procainamide will usually slow the tachycardia
rate and improve the hemodynamic state .
 Although retrograde AV node conduction is
usually the weak link during AAVRT,
intravenously administered AV node-specific
blocking drugs such as beta blockers, calcium
channel blockers, adenosine, and digoxin should
be avoided unless the tachycardia is definitely
known to be AAVRT. If the diagnosis is not
certain, the patient should be considered to have
an undiagnosed wide QRS tachycardia; of
particular concern is ventricular tachycardia,
which can become hemodynamically unstable or
even degenerate into ventricular fibrillation
following administration of one of these drugs.
 These drugs should also be avoided in patients with WPW
who have atrial fibrillation, since blocking the AV node will
promote conduction down the accessory pathway. Another
problem is that AAVRT can also degenerate into AF
following drug administration, especially with adenosine .
In either case, inhibition of AV node conduction may
enhance the preexcited ventricular rate response.
 Chronic therapy for prevention  — Ablation of the
accessory pathway is the preferred therapy for chronic
prevention of AAVRT. An important concern about long-
term medical therapy of this arrhythmia is the potential
for AF. The accessory pathway, which is the antegrade
limb, is also capable of antegrade preexcited conduction
during AF.
 The selection of an effective antiarrhythmic
drug should be based upon the effect of the
drug on the electrophysiologic properties of the
various parts of the reentrant circuit and on the
ability to induce the arrhythmia. The AV nodal
blocking agents, beta blockers, calcium channel
blockers,and digoxin arecontraindicated because
of the possible occurrence of atrial fibrillation
with accelerated conduction down the accessory
pathway.
 Procainamide depresses conduction and prolongs
refractoriness in atrial and ventricular
myocardium, accessory pathways, and the His-
Purkinje system, while having no effect or
causing slight shortening of AV nodal refractory
period 
TREATMENT
 Patients with a history of recurrent symptomatic
SVT episodes, incessant SVT, and heart rates
>200 beats/min with SVT should be given strong
consideration for undergoing catheter ablation

 Patients who demonstrate evidence of

ventricular preexcitation in the absence of any
prior arrhythmia history merit special
consideration.
TREATMENT
Recommendations
Catheter ablation in patients Class I - Procedure should be
resuscitated from sudden cardiac performed
arrest due to atrial fibrillation and
rapid condunction over the
accessory pathway causing
ventricular fibrillation)

Catheter ablation in symptomatic Class IIa - Procedure is

patients WPW syndrome who have reasonable
accessory pathways with
refractory periods less than 240
ms in duration
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