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Wolff-Parkinson-White syndromeHighlights
Summary
Overview
Basics
Definition
EpidemiologyAetiology
Pathophysiology
Classification
Prevention
Screening
Diagnosis
History & examination
Tests
Differential
Step-by-step
Criteria
GuidelinesCase history
Treatment
Details
Step-by-step
Guidelines
Follow Up
Recommendations
Complications
Prognosis
Resources
References
Images
Patient leaflets
Credits
Feedback
Share
Add to Portfolio
Bookmark
Add notes
History & exam
Key factors
presence of risk factors
atrioventricular re-entrant tachycardia (AVRT)
Other diagnostic factors
palpitations
dizziness
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SOB
chest pain
atrial fibrillation
atrial flutter
sudden cardiac death (SCD)
syncope and presyncope
tachycardia in pregnancy
congenital cardiac abnormalities
History & exam details
Diagnostic tests
1st tests to order
12-lead ECG
Tests to consider
echocardiogram
treadmill exercise test
pharmacological testing with procainamide or ajmaline
electrophysiology study
Diagnostic tests details
Treatment details
Presumptive
unstable: BP
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stable: pre-excited tachycardia due to atrial fibrillation or atrial flutter
anti-arrhythmics + consider anticoagulation
rapid atrial pacing (for atrial flutter)
DC cardioversion
stable: pre-excited tachycardia due to atrial tachycardia
anti-arrhythmics
rapid atrial pacing
DC cardioversion
Ongoing
following acute treatment: asymptomatic
risk stratification and monitoring
catheter ablation
following acute treatment: minimally symptomatic
monitoring + vagal manoeuvre education (for orthodromic AVRT)
catheter ablation
pharmacological therapy
following acute treatment: symptomatic
catheter ablation
anti-arrhythmics
beta-blockers
Treatment details
Summary Myocardial fibres from the atrium to the ipsilateral ventricle across the mitral or tricuspid annulus
(accessory pathway) cause the ventricle to become pre-excited.
WPW syndrome is usually restricted to symptomatic patients with a typical ECG abnormality; WPW
pattern signifies an asymptomatic patient with typical ECG abnormalities.
Patients often present with AV re-entrant tachycardia or atrial fibrillation and, rarely, sudden cardiac
death.
Asymptomatic patients, except for those with specialised jobs (e.g., airline pilot, school bus driver),
should not be treated but can be monitored for symptoms.
Minimally symptomatic patients may be treated with catheter ablation or medical therapy or only during
the rare symptomatic episodes.
Symptomatic patients usually undergo catheter ablation as a first-line therapy.
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Catheter ablation has a high efficacy and low risk and can be used either as initial therapy or for patients
experiencing side effects or arrhythmia recurrence during drug therapy.
DefinitionOccurs when one or more strands of myocardial fibres capable of conducting
electrical impulses (known as accessory pathways [APs] or bypass tracts)connect the atrium to the ipsilateral ventricle across the mitral or tricuspidannulus.[1] Conduction from the atrium reaches the adjacent ventricle earliervia the AP, which normally has no conduction delay, and a part of theventricle is pre-excited. The term "Wolff-Parkinson-White (WPW) syndrome"is usually restricted to symptomatic patients with a typical ECG abnormality,whereas the term "WPW pattern" signifies an asymptomatic patient withtypical ECG abnormalities.[2]
EpidemiologyThe exact prevalence of pre-excitation syndrome is difficult to estimatebecause most patients are asymptomatic. Intermittent pre-excitation and lossof pre-excitation over time also precludes accurate estimation of itsprevalence. The prevalence of WPW-pattern ECG in the general populationis 0.1% to 0.3%.[3] [4] The yearly incidence is 0.004% to 0.1% (50% of theseare asymptomatic). The male-to-female ratio is 2:1.[5] [6] Signs of pre-excitation were absent in the initial ECG in 22% of subjects with WPW-pattern ECG and 40% of these lost pre-excitation in subsequent ECG
recordings.[5] The prevalence of WPW syndrome varies with the populationstudied. In a review of 22,500 healthy aviation personnel, the WPW patternwas seen in 0.25%; however, only 1.8% of these patients had documentedarrhythmia. It can be encountered at any age, but the highest incidence is inthe third and fourth decades of life.[7]In a report of 228 subjects with WPWsyndrome, the overall incidence of arrhythmia was 1% per year during a 22-year follow-up.
AetiologyWPW pattern on ECG arises from a developmental cardiac defect in the AV
electrical insulation at the AV groove due to the presence of an AP. TheseAPs are usually single epicardial strands of tissue that travel across the AVgroove to connect the atrium and the adjacent ventricular myocardium. Viewimage Less commonly, they are multiple hair-like strands or a broad band oftissues. Rarely, these muscle bands extend over coronary sinus diverticula ormay connect right atrial appendage to the anterior right ventricle. Theincidence of an AP is 40% to 60% on the left free wall, 20% on the right or left
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posteroseptal area, 13% to 21% on the right free wall, and 2% to 10% on theanteroseptal area.
Common locations of accessory pathways (APs) across the mitral and tricuspid
annuliFrom the collection of Dr Mithilesh K. DasUnlike the AV node, whereconduction slows at faster rates of stimulation or rapid atrial rates(decremental conduction), approximately 90% of these APs are rapidlyconducting (presumably because of INa+ dependent conduction), resulting incircus movement tachycardia involving the atrium and ipsilateral ventricle withthe AP as one limb and AV node as another limb of the circuit (AV re-entranttachycardias). Approximately 10% of the APs in WPW syndrome are slowly
conducting (AV node-like property, perhaps ICa+ dependent).The presence of these APs can be associated with various disorders.Ebstein's anomaly is a malformation of the tricuspid valve and right ventriclecharacterised by adherence of the septal and posterior tricuspid leaflets tothe underlying myocardium, apical displacement of the tricuspid annulus anddilation of the atrialised portion of the right ventricle. View image Other rareassociations include hypertrophic cardiomyopathy, mitral valve prolapse,atrial septal defect, ventricular septal defect, transposition of the greatvessels, coarctation of the aorta, dextrocardia, coronary sinus diverticula,
right and left atrial aneurysms, cardiac rhabdomyomas (as seen in patientswith tuberous sclerosis), Marfan's syndrome, and Friedreich's ataxia. ViewimageThe incidence of multiple APs (2 to 5) in patients with WPW syndrome is 5%to 13%.[8] The frequency of multiple APs in left lateral, right lateral, andseptal areas are 44%, 33%, and 22%, respectively. It is more common inpatients with a family history of WPW syndrome and in patients with Ebstein'sanomaly or other congenital heart diseases (10% to 20%).[9] Multiple APs
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are associated with a higher incidence of antidromic reciprocating tachycardia(ART) and a higher incidence of sudden cardiac death (SCD).
PathophysiologyNormal conduction from the atria to the ventricles occurs via the AV node
(where minor physiological delay occurs) and through the His-Purkinjesystem, resulting in a normal PR interval and a narrow QRS complex. InWPW syndrome, because of the physiological delay of conduction in the AVnode, conduction from the atrium reaches the adjacent ventricle earlier viathe AP, which normally has no conduction delay, and a part of the ventricle ispre-excited, resulting in a slurred upstroke at the initiation of the QRScomplex, known as the delta wave. Therefore, the QRS complexes are thefusion of the normal ventricular depolarisation via the AV node-His bundleand the depolarisation of a part of the ventricle via the AP.
The degree of pre-excitation depends upon the relative contribution of theimpulse via the AP versus the AV node. Conduction over the AP results inshortening of the PR interval (110 ms) with secondary ST-T wave changes. View image These APs in theWPW syndrome are usually capable of conducting bidirectionally (atrium toventricle and ventricle to atrium). When an AP is capable of retrogradeconduction only (from the ventricle to the atria), the ECG is normal and nodelta wave is seen (concealed AP). View image These APs serve as asubstrate for re-entry and can cause a supraventricular tachycardia (SVT)
involving the AV node as the other connection between the atrium and theventricle. This type of SVT is termed AVRT. During atrial fibrillation (AF),which occurs in up to one third of WPW syndrome patients, the AP canconduct rapidly to the ventricle, rarely causing ventricular fibrillation (VF) thatmay result in sudden cardiac death (SCD).
AVRT: AVRT is the most common arrhythmia, which occurs in approximately 70% to 80% of the
symptomatic patients with WPW syndrome. The common form of AVRT involves impulse conduction via the AV
node, down the His-Purkinje system to the ventricles anterogradely, and the AP retrogradely, resulting in rapid
atrial activation after ventricular depolarisation. This is known as orthodromic reciprocating tachycardia (ORT).
Less commonly (5% to 10%), AVRT results from impulse conduction in a direction opposite to ORT: that is,
conduction from atrium to ventricle via the AP and then from the ventricle to the atrium via the His-Purkinje
system and the AV node. Therefore, it is a regular wide complex tachycardia (WCT), because ventricular
activation is transmyocardial rather than via the specialised conduction tissue. This type of AVRT is known as
antidromic reciprocating tachycardia (ART). View image
ORT: AVRT occurs in 70% to 80% of patients with WPW syndrome. During ORT, the impulses reach the
ventricles via the normal conduction system (AV node and His-Purkinje system) and then return to the atrium via
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the AP as soon as ventricular depolarisation reaches the valve annuli. Tachycardia more commonly starts after a
premature atrial complex that blocks at the refractory AP but is able to conduct down the AV node to the
ventricles. By this time, the AP recovers and the impulse reaches the atrium via the AP and then travels to the
ventricles via the AV node, to continue as ORT.View imageDuring ORT the ventricle is depolarised via the
normal conduction system; ORT is a narrow complex tachycardia with a short RP` interval (short RP`
tachycardia). View image ART: ART is a less common arrhythmia in WPW syndrome patients. The common mechanism of
initiation of the ART is by a premature atrial complex. View image The impulse is blocked at the AV node if it is
refractory but conducts down the AP to the ventricles and then back to the atrium via the AV node, and then the
circus movement tachycardia is initiated. The baseline ECG (upper panel) of a patient with minimum pre-
excitation and the WCT (lower panel) is an ART with negative delta wave in inferior leads and lead V1
suggestive of a right inferoseptal AP as shown here. View image The ART is a wide QRS tachycardia and
therefore can be confused with a ventricular tachycardia (VT) or an SVT with aberrancy. The baseline ECG is
the key in most cases. If there is positive QRS concordance (QRS polarity positive in all precordial leads due to
annular location of the APs) during ART, then this may mimic a VT. However, if there is negative concordance(QRS polarity negative in all precordial leads), then an ART is ruled out - except for a rare AVRT involving an
atriofascicular pathway, which has AV node-like property that connects the tricuspid annulus to the distal right
bundle and results in a left bundle branch block configuration WCT.
AF: AF is encountered in 10% to 35% of patients with WPW syndrome. AF with rapid conduction via the
AP is recognised by an irregular WCT with a varying degree of ventricular pre-excitation. Patients with a rapidly
conducting AP or multiple APs are at a risk for VF due to rapid ventricular stimulation. View image
Atrial flutter and atrial tachycardia: Atrial flutter and atrial tachycardia can result in a regular pre-excited
WCT. Atrial flutter is encountered in 5% to 10% of patients with WPW syndrome. If the conduction is rapid,
especially during atrial flutter with 1:1 AV conduction, then rapid stimulation of ventricle can also result in VF. AVnodal Wenckebach pattern over the AV node or the AP in atrial flutter and AF can result in an irregular
WCT. View image
Classification
Manifest accessory AP versus concealed AP
APs in WPW syndrome are usually capable of conducting bidirectionally(atrium to ventricle and ventricle to atrium). When an AP is capable ofconducting retrogradely only (from the ventricle to the atria), the ECG is
normal and no delta wave is seen (concealed AP). View image These APsserve as a substrate for re-entry and can cause a supraventriculartachycardia (SVT) involving the AV node as the other connection between theatrium and the ventricle. This type of SVT is termed atrioventricular re-entranttachycardia (AVRT).
Asymptomatic/minimally symptomatic/symptomatic patients
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Minimally symptomatic patients are those with brief, well-tolerated episodesof symptoms (usually fewer than 5 episodes per year of non-pre-excitedSVT). Symptomatic patients can be considered as those with episodes lesswell tolerated by the patient. Tolerance is subjective by the patient.
AV re-entrant tachycardia (AVRT)AVRT is the most common arrhythmia, which occurs in approximately 70% to80% of the symptomatic patients with WPW syndrome.
Orthodromic reciprocating tachycardia (ORT): during ORT the ventricle isdepolarised via the normal conduction system; ORT is a narrow complextachycardia with a short RP` interval (short RP` tachycardia). ViewimageView image
Antidromic reciprocating tachycardia (ART): the ART is a wide QRStachycardia. View image
ScreeningFamily members are not commonly screened.
History & examinationKey diagnostic factorshide allpresence of risk factors (common)
Key risk factors are congenital cardiac abnormalities. The most common is Ebstein's anomaly.
atrioventricular re-entrant tachycardia (AVRT) (common)
The most common arrhythmia is AVRT, which occurs in approximately 70% to 80% of patients.Other diagnostic factorshide allpalpitations (common)
Presenting feature of an acute arrhythmia due to WPW.
dizziness (common)
Presenting feature of an acute arrhythmia due to WPW.
SOB (common)
Presenting feature of an acute arrhythmia due to WPW.
chest pain (common)
Presenting feature of an acute arrhythmia due to WPW.
atrial fibrillation (common)
Atrial fibrillation and flutter occur alone in 16% of patients and in 20% of patients with AVRT.
Typically the heart rate varies between 150 and 240 bpm.atrial flutter(common)
Atrial fibrillation and flutter occur alone in 16% of patients and in 20% of patients with AVRT.
Typically the heart rate varies between 150 and 240 bpm.congenital cardiac abnormalities (common)
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From 7% to 20% of patients with WPW syndrome have other accompanying congenital
abnormalities. The most common is Ebstein's anomaly, which is associated with single or multiple
right-sided APs.sudden cardiac death (SCD) (uncommon)
The following factors are considered high risk for SCD, especially in patients with a history of
syncope: fastest rate 225 bpm during atrial fibrillation; anterograde refractory period 270 ms;
multiple APs.syncope and presyncope (uncommon)
Usually with a history of palpitations and dizziness. Syncope is an uncommon presentation
(incidence
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coarctation of aorta
Less commonly, patients with WPW syndrome may have other accompanying congenital
abnormalities.dextrocardia
Less commonly, patients with WPW syndrome may have other accompanying congenital
abnormalities.coronary sinus diverticula
Less commonly, patients with WPW syndrome may have other accompanying congenital
abnormalities.right and left atrial aneurysms
Less commonly, patients with WPW syndrome may have other accompanying congenital
abnormalities.cardiac rhabdomyomas
Seen in patients with tuberous sclerosis.
Marfan's syndrome
Occasionally associated with WPW syndrome.
Friedreich's ataxia
Occasionally associated with WPW syndrome.
family history
The incidence of familial WPW syndrome among patients with APs is reported to be 3.4% and the
prevalence in first-degree relatives is 0.55%.[7] [10]Autosomal dominant inheritance is also
reported. Familial forms have a higher incidence of multiple APs, but usually do not have male
preponderance or structural cardiac abnormalities. Rare inherited disorders are also associated
with familial WPW syndrome.[11]Diagnostic tests1st tests to orderhide all
Test
12-lead ECG
ECG should be recorded in any patients with suspected supraventricular arrhythmia. Intermittent pre-exc
by the electrocardiographic presence of QRS complexes with pre-excitation intermingled with narrow QR
to conduction solely via the AV node (without pre-excitation). Sometimes, pre-excited QRS complexes a
narrow QRS complex because of a long refractory period of the AP. View image Intermittent pre-excitati
the AP is incapable of conduction to the ventricle fast enough to pose a risk for ventricular fibrillation dur
arrhythmias such as atrial fibrillation or flutter. An algorithm of delta wave polarity in 12-lead ECG or duri
tachycardia has been developed. View image
Twelve-lead ECG at baseline shows no delta waves and short RP` tachycardia during the clinical arrhyth
re-entrant tachycardia.
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Tests to considerhide all
Test
echocardiogram
Risk of associated heart disease is 7% to 20%.
treadmill exercise test
An important indicator of a low risk of sudden cardiac death is the disappearance of pre-excitation during
to a long anterograde refractory period of the AP.[14] Sympathetic stimulation occurring during exercise
refractory period of the AP and if the refractory period of the AP is reached, then the conduction down th
blocked. This indicates that during atrial fibrillation, conduction down the AP will not be fast enough to ca
fibrillation.pharmacological testing with procainamide or ajmaline
Pharmacological testing is performed with IV procainamide (10 mg/kg over 5 minutes) or ajmaline (1 mg
minutes). Both drugs prolong the refractory period of the AP. If pre-excitation is abolished during or after
most probably indicates a low risk for SCD. These anti-arrhythmic drugs prolong the refractory period of
system and may cause complete heart block. Additionally, these drugs can provoke torsades de pointes
patients. Therefore, these drugs should be used in a monitored setting and the patients should be discha
only after 4 to 5 hours of monitoring.
electrophysiology study
Risk stratification is performed invasively by programmed electrical stimulation with intracardiac recordin
semi-invasive atrial stimulation by trans-oesophageal route.[15] [16] [14] [17]
Differential diagnosis
Condition
Differentiating
signs/symptoms Differentiating tests
Atriofascicular pathway There may
be no
differencein signs
and
symptoms
in acute
presentatio
n with
Baseline ECG normal. On electrophysiological study, the p
lateral tricuspid annulus to right ventricular apex.
Arrhythmias not seen are: orthodromic atrioventricular re-e
fibrillation and flutter, and long RP` tachycardia. View imag
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arrhythmia
s.
Lown-Ganong-Levine
syndrome There may
be nodifference
in signs
and
symptoms
in acute
presentatio
n with
arrhythmia
s.
Baseline ECG shows short PR interval. On electrophysiolo
bypass or enhanced AV nodal conduction.
Arrhythmias not seen are: antidromic AVRT, atrial fibrillatio
tachycardia.
Nodofasicular pathway There may
be no
difference
in signs
and
symptoms
in acute
presentatio
n with
arrhythmia
s.
Baseline ECG shows short PR interval, but no delta wave.
there will be a pathway from atrioventricular node to the ve
Arrhythmias not seen are: orthodromic AVRT, antidromic A
and long RP` tachycardia. View image
Fasciculoventricular
pathway There may
be no
difference
in signs
and
symptoms
in acute
presentatio
n with
arrhythmia
Baseline ECG shows short PR, narrow QRS, and delta wav
study, there will be a His bundle or bundle branch to the ve
Arrhythmias not seen are: orthodromic AVRT, antidromic A
and long RP` tachycardia. View image
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s.
Other APs with atypical
course There may
be no
differencein signs
and
symptoms
in acute
presentatio
n with
arrhythmia
s.
Baseline ECG shows delta wave. Electrophysiology shows
atrial appendage to ventricle. View image
Step-by-step diagnostic approachIt is common to have WPW pattern as an incidental finding in healthy peoplewho have ECG recording done for a routine health check-up. A 12-lead ECGshowing delta waves signifies APs capable of conducting anterograde. In themajority of patients these APs are capable of retrograde conduction aswell. View image
Acute presentationsPatients with an acute arrhythmia due to WPW may present with palpitations,dizziness, shortness of breath, and chest pain. The most commonarrhythmias diagnosed are atrioventricular re-entrant tachycardia (AVRT),atrial fibrillation, and atrial flutter. Sudden cardiac death and syncope andpresyncope are associated outcomes but rare. ECG should be recorded inany patients with suspected supraventricular arrhythmia.
Congenital cardiac abnormalities
From 7% to 20% of patients with WPW syndrome have other accompanyingcongenital abnormalities, the most common being Ebstein's anomaly, whichis associated with single or multiple right-sided APs. View image Other rareassociations include hypertrophic cardiomyopathy, View image mitral valveprolapse, atrial septal defect, ventricular septal defect, transposition of thegreat vessels, coarctation of the aorta, dextrocardia, coronary sinusdiverticula, right and left atrial aneurysms, cardiac rhabdomyomas (as seen in
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patients with tuberous sclerosis), Marfan's syndrome, and Friedreich's ataxia.Echo can be used to diagnose these.
Locating APsThe precise localisation of these APs helps in assessing the success rate and
risks for catheter ablation, and in planning the ablation strategy. For example,left-sided APs are often ablated via a transseptal approach, and paraseptal
APs, which are close to the His bundle, are associated with a high risk forcomplete AV block during catheter ablation (some electrophysiologists nowprefer cryoablation for APs close to the His bundle; see the treatmentsection).
Several algorithms have been developed, but, as a general rule, a positivedelta wave (first 40 ms of QRS complex) in lead V1 suggests a left-sided AP
and a negative delta wave in V1 suggests a right-sided AP. View image Apositive delta wave in inferior lead with inferior axis represents anteroseptal
AP. View image A left axis (with a negative delta wave in lead V1) suggests aright lateral AP. If the delta waves in the inferior leads are negative, then itdenotes a posteroseptal AP right or left, depending on the delta wave vectorin lead V1 as described above. View image A negative delta wave in lead I,aVL, and V6 (rightward QRS axis) with a positive delta wave in lead V1suggests a left lateral pathway. It is prudent to recognise that the delta wavevector can only be determined with precision when the ECG shows maximum
pre-excitation. A right-sided AP with minimal pre-excitation but with aposteroseptal location cannot be determined with a high probability until ARToccurs. View image
Risk stratificationPatients with WPW pattern should be risk stratified with non-invasive andinvasive tests, and those who are low risk should be monitored for any futurearrhythmia. Since non-invasive tests are considered inferior to invasiveelectrophysiological assessment for risk of sudden cardiac death, some
electrophysiologists feel that some asymptomatic patients warrant invasiverisk stratification. Therefore, asymptomatic patients should be referred to anelectrophysiologist or a cardiologist with expertise in arrhythmia evaluation forrisk stratification. While controversy exists, most experts recommend that allpatients with ventricular pre-excitation undergo risk stratification to determinetheir risk of sudden cardiac death, regardless of the presence ofsymptoms.[12] [13] The risk of sudden cardiac death is determined by the
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anterograde refractory period of the accessory pathway. If the refractoryperiod is very short, patients are at risk for developing ventricular fibrillation inthe setting of atrial fibrillation conducting rapidly over the accessory pathway.If ventricular pre-excitation is intermittent at rest, then the accessory pathwayis low risk for causing sudden cardiac death. If ventricular pre-excitation is
always present at rest, patients should undergo exercise treadmill testinglooking forabrupt loss of pre-excitation, again indicative of an accessorypathway incapable of dangerously rapid conduction from the atrium to theventricle. If pre-excitation does not abruptly disappear with exercise, theninvasive risk stratification at electrophysiology study should be considered.
Accessory pathways capable of rapid anterograde conduction should beablated to reduce the risk of sudden cardiac death, regardless of whether ornot they cause supraventricular tachycardia.Intermittent pre-excitation occurs due to age-related degeneration of the APs,
and usually these pathways have a longer refractory period. It is alsoimportant to note that left lateral pathways may not be able to pre-excite theleft ventricle earlier than the arrival of the impulse via the normal route due toits distance from the sinus node. Therefore, the baseline ECG may beunremarkable with a normal PR interval and no delta wave on the ECG.These pathways become manifest only when AV nodal conduction isrelatively slow due to altered autonomic tone, rapid atrial rate due to sinustachycardia (such as during exercise), or atrial arrhythmias (latent WPWsyndrome). The ECG of a patient with minimal pre-excitation who developed
an AVRT is shown here. View image View imageA treadmill exercise test can be used as an indicator of risk of suddendeath. View image View image View image
Click to view diagnostic guideline references. Diagnostic criteria
WPW syndrome versus WPW-pattern ECG
WPW syndrome or pre-excitation syndrome occurs when one or more strands of myocardial fibres capable of
conducting electrical impulses (known as APs or bypass tracts) connect the atrium to the ipsilateral ventricle
across the mitral or tricuspid annulus.[1]A patient who is asymptomatic but with typical WPW ECG
abnormalities is referred to as having WPW pattern.
Asymptomatic/minimally symptomatic/symptomatic patients
Minimally symptomatic patients are those with brief well-tolerated episodes of symptoms (usually fewer than 5
episodes per year of non-pre-excited SVT). Symptomatic patients can be considered as those with episodes less
well tolerated by the patient. Tolerance is subjective by the patient.
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Case history #1A 42-year-old man complains of palpitations following dizziness and a briefloss of consciousness. His wife reports that he is pale and short of breath.Emergency medical services were called and found him pulseless. The ECG
revealed a rapid, irregular wide complex tachycardia. Later he wassuccessfully resuscitated with two successive DC shocks.
Case history #2A 35-year-old man presents to an ER with palpitation, SOB, dizziness, andchest pain of 4 hours' duration. An ECG demonstrated narrow-complex shortRP` tachycardia that responded to IV adenosine. The ECG during sinusrhythm revealed signs of pre-excitation.
Other presentationsAsymptomatic people are sometimes diagnosed during a routine physicalexamination. The most common age of the presentation is adolescence andearly adulthood (in third and fourth decades); however, it can occur at anyage. There can be a long-standing history of palpitations lasting for minutesto hours.
Treatment Options
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unstable: BP
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unstable: BP
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line Treatmenthide all
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line Treatmenthide all
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line Treatmenthide all
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Patient group
Treatment
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following acute treatment:
asymptomatic
1st risk stratification and monitoring
While controversy exists, most experts recommend
that all patients with ventricular pre-excitation
undergo risk stratification to determine their risk of
sudden cardiac death, regardless of the presence
of symptoms.[12] [13]
Asymptomatic patients, except for those in
specialised jobs with particular safety issues,
should not be treated but can be monitored for
symptoms by visits to a physician around every 2
years.
adjunct
[?]
catheter ablation
Asymptomatic patients in specialised jobs with
particular safety issues (e.g., airline pilot, school
bus driver) can be considered for catheter
ablation.[18]
following acute treatment:
minimally symptomatic
1st monitoring + vagal manoeuvre education (for orthodromic
AVRT)
These are patients who have a single, well-
tolerated, non-pre-excited supraventricular
tachycardia (SVT) episode, or those who regularly
have fewer than 5 SVT episodes a year, also well-
tolerated and non-pre-excited.
Patients require monitoring with visits to a
physician about every 2 years.
Patients with orthodromic AV reciprocating
tachycardia (narrow complex tachycardia) can be
taught vagal maneuvers (e.g., Valsalva) to stop
episodes of SVT.
1st catheter ablation
Catheter ablation has a high efficacy and low risk,
and can be used either as initial therapy or for
patients experiencing side effects or arrhythmia
recurrence during drug therapy. It is often a matter
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Patient group
Treatment
line Treatmenthide all
following acute treatment:
asymptomatic
1st risk stratification and monitoring
While controversy exists, most experts recommend
that all patients with ventricular pre-excitation
undergo risk stratification to determine their risk of
sudden cardiac death, regardless of the presence
of symptoms.[12] [13]
Asymptomatic patients, except for those in
specialised jobs with particular safety issues,
should not be treated but can be monitored for
symptoms by visits to a physician around every 2
years.
of patient choice, and is useful in those with
specialised jobs that require consciousness (e.g.,
school bus driver, airline pilot).[18]
2nd pharmacological therapy
Those whose episodes are not sufficiently
controlled by vagal manoeuvres can carry the pill-
in-the-pocket (propranolol and diltiazem) to take at
the onset of symptoms of a non-pre-excited
tachycardia. Other versions include propafenone or
flecainide along with metoprolol or diltiazem.
Class I anti-arrhythmic agents (fleicanide or
propafenone) are suitable for patients with no
additional cardiac disease but cannot be used in
people with CAD or structural heart disease.
In patients with CAD or structural heart disease,
class III anti-arrhythmic agents (sotalol,
amiodarone, or dofetilide) may be used.
Verapamil and diltiazem should not be used as the
sole therapy for patients with accessory pathways
that might be capable of rapid conduction during
AF. This concern also applies to digoxin, which
also should not be used in this situation.
QT interval must be determined prior to starting
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Patient group
Treatment
line Treatmenthide all
following acute treatment:
asymptomatic
1st risk stratification and monitoring
While controversy exists, most experts recommend
that all patients with ventricular pre-excitation
undergo risk stratification to determine their risk of
sudden cardiac death, regardless of the presence
of symptoms.[12] [13]
Asymptomatic patients, except for those in
specialised jobs with particular safety issues,
should not be treated but can be monitored for
symptoms by visits to a physician around every 2
years.
therapy with dofetilide as it is contraindicated if QTc
is >440 msec (>500 msec in patients with
ventricular conduction abnormalities).
Primary Options
pill-in-the-pocket
propranolol: 80 mg orally (immediate-release) as a
single dose
and
diltiazem: 120 mg orally (immediate-release) as a
single dose
OR
pill-in-the-pocket
propafenone : 450-600 mg orally (immediate-
release) as a single dose
or
flecainide: 200-300 mg orally as a single dose
-- AND --
metoprolol : 50 mg orally (immediate-release) as a
single dose
or
diltiazem: 120 mg orally (immediate-release) as a
single dose
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Patient group
Treatment
line Treatmenthide all
following acute treatment:
asymptomatic
1st risk stratification and monitoring
While controversy exists, most experts recommend
that all patients with ventricular pre-excitation
undergo risk stratification to determine their risk of
sudden cardiac death, regardless of the presence
of symptoms.[12] [13]
Asymptomatic patients, except for those in
specialised jobs with particular safety issues,
should not be treated but can be monitored for
symptoms by visits to a physician around every 2
years.
Secondary Options
flecainide: 50-150 mg orally twice daily
OR
propafenone : 150-300 mg orally (immediate-
release) every 8 hours
Tertiary Options
sotalol : 80-160 mg orally twice daily
OR
amiodarone: 600-800 mg/day orally given in 2
divided doses as a loading dose for 2 weeks,
followed by maintenance dose of 200-400 mg/day
OR
dofetilide : 125-500 micrograms orally twice daily
following acute treatment:
symptomatic
1st catheter ablation
All patients should be offered catheter ablation.
2nd anti-arrhythmics
Used in patients who refuse ablation or in whom
ablation is unsuitable.
Class I anti-arrhythmic agents (fleicanide or
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Patient group
Treatment
line Treatmenthide all
following acute treatment:
asymptomatic
1st risk stratification and monitoring
While controversy exists, most experts recommend
that all patients with ventricular pre-excitation
undergo risk stratification to determine their risk of
sudden cardiac death, regardless of the presence
of symptoms.[12] [13]
Asymptomatic patients, except for those in
specialised jobs with particular safety issues,
should not be treated but can be monitored for
symptoms by visits to a physician around every 2
years.
dofetilide : 125-500 micrograms orally twice daily
adjunct
[?]
beta-blockers
Beta-blockers can be given to patients who find
that they need additional control of symptoms.
Primary Options
atenolol : 50-200 mg/day orally given in 1-2 divided
doses
OR
metoprolol : 25-100 mg orally twice daily
Ongoing
Treatment approachTreatment of acute presentations is based on the nature of the arrhythmia.Ongoing treatment is decided according to the symptoms of the patient, as
well as risk stratification for sudden cardiac death.
AsymptomaticWhile controversy exists, most experts recommend that all patients withventricular pre-excitation undergo risk stratification to determine their risk ofsudden cardiac death, regardless of the presence of symptoms.[12] [13] Therisk of sudden cardiac death is determined by the anterograde refractory
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period of the accessory pathway. If the refractory period is very short,patients are at risk for developing ventricular fibrillation in the setting of atrialfibrillation conducting rapidly over the accessory pathway. If ventricular pre-excitation is intermittent at rest, then the accessory pathway is low risk forcausing sudden cardiac death. If ventricular pre-excitation is always present
at rest, patients should undergo exercise treadmill testing looking for abruptloss of pre-excitation, again indicative of an accessory pathway incapable ofdangerously rapid conduction from the atrium to the ventricle. If pre-excitationdoes not abruptly disappear with exercise, then invasive risk stratification atelectrophysiology study should be considered. Accessory pathways capableof rapid anterograde conduction should be ablated to reduce the risk ofsudden cardiac death, regardless of whether or not they causesupraventricular tachycardia (SVT).
Minimally symptomaticThese are patients who have a single, well-tolerated, non-pre-excitedsupraventricular tachycardia episode, or those who regularly have fewer than5 SVT episodes a year, also well-tolerated and non-pre-excited. Patientsrequire monitoring with visits to a physician about every 2 years.
Patients with orthodromic AV reciprocating tachycardia (narrow complextachycardia) can be taught vagal maneuvers (e.g., Valsalva) to stop episodesof SVT. All minimally symptomatic patients requiring further treatment can
carry the pill-in-the-pocket (propranolol and diltiazem) to take at the onset ofsymptoms of a non-pre-excited tachycardia. Other versions includepropafenone or flecainide along with metoprolol or diltiazem.
Minimally symptomatic patients may be treated with catheter ablation ormedical therapy or only during the rare symptomatic episodes. Decision totreat should be based on patients' concern about their own symptoms.Catheter ablation has a high efficacy and low risk, and can be used either asinitial therapy or for patients experiencing side effects or arrhythmiarecurrence during drug therapy.
Symptomatic patientsSymptomatic patients usually undergo catheter ablation as a first-linetherapy.
Anti-arrhythmic drugs are one of the therapeutic options for the managementof symptomatic WPW syndrome, but they have been increasingly replaced by
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catheter ablation. The choice between drugs and ablation is often down to thepreference of the patients and whether they wish to go through theprocedure. Although there have been no controlled trials of drug prophylaxisinvolving symptomatic WPW syndrome, drugs are recommended on thebasis of the safety and efficacy of these anti-arrhythmic drugs reported in a
number of small, non-randomised trials (each involving
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Adenosine is preferred because of its ultra-short half-life (
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Pre-excited tachycardia results in a rapid irregular wide complex tachycardiawith varying duration and amplitude of QRS complexes depending upon thedegree of pre-excitation. View image IV infusions of anti-arrhythmic drugssuch as procainamide, ibutilide, flecainide, or amiodarone, which preventrapid conduction through the AP, are used, even though they may not be able
to terminate the atrial arrhythmia.[15]Anticoagulation should be considered in atrial fibrillation and atrial flutterdepending on presence of co-morbid cardiologic abnormalities and durationof onset.
In atrial tachycardia or atrial flutter, rapid atrial pacing using a temporarypacemaker for overdrive suppression of the tachycardia or flutter can be usedif the previous drug treatments fail. However, it is more effective in atrialtachycardia than atrial flutter since the atrial rate is slower in atrial
tachycardia. Rapid atrial pacing has no role in atrial fibrillation.DC cardioversion can be used when symptoms persist in patients or if thepatient becomes haemodynamically unstable. However, the recurrence ofatrial arrhythmia after DC cardioversion may be higher in atrial tachycardia,compared to atrial fibrillation/flutter, depending on the mechanism. If the atrialtachycardia is related to abnormal automaticity, DC cardioversion may not beeffective at all, such as multifocal atrial tachycardia (MAT).
MonitoringPatients should visit their physician every 2 to 3 years for monitoring.
Patient InstructionsPatients should visit their physician every 2 to 3 years for monitoring.
Patients should call the emergency services if they have any recurrence ofsymptoms.
In minimally symptomatic patients who have a single, well-tolerated, non-pre-excited supraventricular tachycardia (SVT) episode, or those who regularlyhave fewer than 5 SVT episodes a year, also well-tolerated and non-pre-excited, these patients can be taught vagal maneuvers (e.g., Valsalva) tostop episodes of SVT.
Those requiring further treatment can carry the pill-in-the-pocket (propranololand diltiazem) to take at the onset of symptoms of a non-pre-excited
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