Highlights & Basics
- Wolff-Parkinson-White (WPW) syndrome occurs when myocardial fibers connect the atrium to the ipsilateral ventricle across the mitral or tricuspid annulus (accessory pathway), pre-exciting the ventricle.
- Patients often present with atrioventricular re-entrant tachycardia, less commonly atrial fibrillation, and, rarely, sudden cardiac death.
- Asymptomatic patients can either be monitored or screened to determine whether they have a "high-risk" accessory pathway, in which case catheter ablation is typically performed. Screening to determine whether a patient has a high-risk accessory pathway is recommended for patients who have high-risk occupations, such as school bus drivers or pilots, and also for competitive athletes. In patients with asymptomatic pre-excitation who have an accessory pathway demonstrating low risk features on invasive or noninvasive screening, an electrophysiology study and ablation can be considered.
- Symptomatic patients usually undergo catheter ablation as first-line therapy. Pharmacologic therapy can be considered for patients in whom catheter ablation fails and also for patients who prefer a noninvasive approach.
- Catheter ablation is highly effective with low risk and can be used either as initial therapy or for patients experiencing side effects or arrhythmia recurrences despite medical treatment.
Quick Reference
History & Exam
Key Factors
atrioventricular re-entrant tachycardia (AVRT)
Other Factors
palpitations
dizziness
shortness of breath
chest pain
atrial fibrillation
atrial flutter
congenital cardiac abnormalities
sudden cardiac death
syncope and presyncope
tachycardia in pregnancy
Diagnostics Tests
1st Tests to Order
12-lead ECG
Other Tests to consider
echocardiogram
treadmill exercise test
electrophysiology study
Treatment Options
presumptive
unstable: BP <90/60 mmHg, signs of systemic hypoperfusion or unstable atrial fibrillation
direct-current (DC) cardioversion
acute
stable: narrow complex (orthodromic atrioventricular reciprocating) tachycardia
carotid sinus massage or Valsalva maneuver
intravenous adenosine or atrioventricular (AV) nodal blocking drugs or antiarrhythmics
rapid atrial pacing
direct-current (DC) cardioversion
Definition
Classifications
Manifest AP versus concealed AP
Asymptomatic/symptomatic patients
Atrioventricular re-entrant tachycardia (AVRT)
Vignette
Common Vignette 1
Common Vignette 2
Other Presentations
Epidemiology
Etiology
Pathophysiology
- AV re-entrant tachycardia (AVRT): AVRT is the most common arrhythmia and occurs in approximately 70% to 80% of patients with WPW syndrome.[3] [4] 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 depolarization. This is known as 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 specialized conduction tissue. This type of AVRT is known as antidromic reciprocating tachycardia (ART). ART is relatively more frequent in patients with multiple APs as compared with those with a single AP and is also relatively less common in patients with septal APs.Image
- ORT: AVRT occurs in 70% to 80% of patients with WPW syndrome.[4] 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 the AP as soon as ventricular depolarization 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. During ORT the ventricle is depolarized via the normal conduction system; ORT is a narrow complex tachycardia with a short RP interval (short RP tachycardia).Images
- ART: ART is a less common arrhythmia in patients with WPW syndrome. ART can be initiated by a premature atrial complex. 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. Alternatively, ART can be initiated by a premature ventricular complex that blocks in the AP and conducts retrograde via the AV node. 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. The ART is a wide QRS tachycardia and therefore can be confused with a ventricular tachycardia (VT) or a supraventricular tachycardia 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.Images
- AF: AF is encountered in 10% to 35% of patients with WPW syndrome. AF with rapid conduction via the AP is recognized 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.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, then rapid stimulation of the ventricle can also result in VF. AV nodal Wenckebach pattern over the AV node or the AP in atrial flutter and AF can result in an irregular WCT.Image
Images
Manifest versus concealed accessory pathway. AP, accessory pathway; AV, atrioventricular; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; SA, sinoatrial
Orthodromic atrioventricular reciprocating tachycardia in a patient with left-sided accessory pathway. AP, accessory pathway; APC, atrial premature complex; AV, atrioventricular; AVRT, atrioventricular re-entrant tachycardia; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; SA, sinoatrial
Orthodromic reciprocating tachycardia induced in a patient with left lateral accessory pathway
Antidromic atrioventricular reciprocating tachycardia in a patient with left-sided accessory pathway. AP, accessory pathway; APC, atrial premature complex; AV, atrioventricular; AVRT, atrioventricular re-entrant tachycardia; LA, left atrium; LV, left ventricle; RA, right atrium; RV, right ventricle; SA, sinoatrial; SVT, supraventricular tachycardia
Antidromic reciprocating tachycardia in a patient with right posteroseptal accessory pathway
Anatomic location of accessory pathways across the valve annuli
Common locations of accessory pathways across the mitral and tricuspid annuli
Right lateral accessory pathway in a patient with Ebstein anomaly
WPW syndrome in a patient with hypertrophic obstructive cardiomyopathy
Collision (fusion) of wave fronts down the atrioventricular node and accessory pathway
Orthodromic and antidromic atrioventricular reciprocating tachycardia circuits. WCT, wide complex tachycardia
Atrial fibrillation in a patient with WPW syndrome with rapid ventricular rate; resulted in aborted sudden cardiac death
Atrial flutter with pre-excitation
A simplified algorithm for localizing an accessory pathway
Left posteroseptal accessory pathway
Right anteroseptal accessory pathway
Resting ECG shows delta waves (red arrows) in the inferior and lateral leads
Loss of pre-excitation (delta waves) in inferior and lateral leads during exercise
Persistent loss of pre-excitation during the recovery period of exercise testing, suggestive of low-risk ECG for sudden cardiac death
Intermittent pre-excitation
Rare forms of accessory pathways occur due to various anatomic substrates with different ECG manifestations
Diagnostic Approach
Acute presentations
Congenital cardiac abnormalities
Locating APs
Risk stratification
- If the refractory period is very short, there are multiple APs, or tachycardia is induced, patients are at risk for developing symptomatic arrhythmias and also ventricular fibrillation in the setting of atrial fibrillation conducting rapidly over the AP. Shorter anterograde refractory periods are associated with an increased risk for sudden cardiac death because the AP can conduct impulses more rapidly to the ventricles. This is particularly important if the patient develops atrial fibrillation. Normally, the ventricles are "protected" from rapid depolarization due to the decremental properties of the AV node. However, in patients with an AP with a short anterograde refractory period, rapid conduction over the AP can lead to rapid ventricular rates that can deteriorate to ventricular fibrillation.
- If ventricular pre-excitation is intermittent at rest, this suggests the anterograde refractory period is relatively long, and the AP is low risk for causing sudden cardiac death.
- If ventricular pre-excitation is always present at rest, patients should be referred to an electrophysiologist to determine whether invasive risk stratification is warranted. If patients do not want to undergo an electrophysiology study, exercise stress testing can be used as a risk stratification tool.
- Abrupt loss of pre-excitation during exercise is indicative of an AP incapable of dangerously rapid conduction from the atrium to the ventricle, and is considered to be a marker of a lower-risk AP. If pre-excitation does not abruptly disappear with exercise, then invasive risk stratification with an electrophysiology study should be considered.
- APs capable of rapid anterograde conduction should be ablated to reduce the risk of sudden cardiac death, regardless of whether or not they cause supraventricular tachycardia.
- A treadmill exercise test can be used as an indicator of risk of sudden death.
Risk Factors
History & Exam
Tests
Differential Diagnosis
Differentiating Signs/Symptoms
- There may be no difference in signs and symptoms in acute presentation with arrhythmias.
Differentiating Tests
- Baseline ECG normal. On electrophysiologic study, the pathway will be located at right lateral tricuspid annulus to right ventricular apex.
- Arrhythmias not seen are: orthodromic atrioventricular re-entry tachycardia (AVRT), atrial fibrillation and flutter, and long RP tachycardia.Image
Differentiating Signs/Symptoms
- There may be no difference in signs and symptoms in acute presentation with arrhythmias.
Differentiating Tests
- Baseline ECG shows short PR interval. On electrophysiologic study, there is atrio-nodal bypass or enhanced atrioventricular nodal conduction.
- Arrhythmias not seen are: antidromic AVRT, atrial fibrillation and flutter, and long RP tachycardia.
Differentiating Signs/Symptoms
- There may be no difference in signs and symptoms in acute presentation with arrhythmias.
Differentiating Tests
- Baseline ECG shows short PR interval, but no delta wave. On electrophysiologic study, there will be a pathway from atrioventricular node to the ventricle.
- Arrhythmias not seen are: orthodromic AVRT, antidromic AVRT, atrial fibrillation and flutter, and long RP tachycardia.Image
Differentiating Signs/Symptoms
- There may be no difference in signs and symptoms in acute presentation with arrhythmias.
Differentiating Tests
- Baseline ECG shows short PR, narrow QRS, and delta wave. On electrophysiologic study, there will be a His bundle or bundle branch to the ventricle.
- Arrhythmias not seen are: orthodromic AVRT, antidromic AVRT, atrial fibrillation and flutter, and long RP tachycardia.Image
Differentiating Signs/Symptoms
- There may be no difference in signs and symptoms in acute presentation with arrhythmias.
Differentiating Tests
- Baseline ECG shows delta wave. Electrophysiology shows a coronary sinus diverticulum or atrial appendage to ventricle.Image
Criteria
Screening
Treatment Approach
Acute management
AV reciprocating tachycardia
Atrial fibrillation, atrial flutter, and atrial tachycardia
Asymptomatic
- If the refractory period is very short, there are multiple APs, or tachycardia is induced, patients are at risk for developing ventricular fibrillation in the setting of atrial fibrillation conducting rapidly over the AP. Shorter anterograde refractory periods are associated with an increased risk for sudden cardiac death because the AP can conduct impulses more rapidly to the ventricles. This is particularly important if the patient develops atrial fibrillation. Normally, the ventricles are "protected" from rapid depolarization due to the decremental properties of the AV node. However, in patients with an AP with a short anterograde refractory period, rapid conduction over the AP can lead to rapid ventricular rates that can deteriorate to ventricular fibrillation.
- If ventricular pre-excitation is intermittent at rest, this suggests the anterograde refractory period is relatively long, and the AP is low risk for causing sudden cardiac death.
- If ventricular pre-excitation is always present at rest, patients should undergo exercise treadmill testing looking for abrupt loss of pre-excitation, again indicative of an AP incapable of dangerously rapid conduction from the atrium to the ventricle. If pre-excitation does not abruptly disappear with exercise, invasive risk stratification with an electrophysiology study should be considered. APs capable of rapid anterograde conduction should be ablated to reduce the risk of sudden cardiac death, regardless of whether or not they cause supraventricular tachycardia. Asymptomatic patients in specialized jobs with particular safety issues (e.g., airline pilot, school bus driver) can also be considered for catheter ablation. Catheter ablation is generally not performed in pregnant patients and should be deferred until after delivery.
Symptomatic patients
Treatment Options
unstable: BP <90/60 mmHg, signs of systemic hypoperfusion or unstable atrial fibrillation
direct-current (DC) cardioversion
Comments
- Patients with an acute tachycardia and who are hemodynamically unstable (BP <90/60 mmHg, with signs of systemic hypoperfusion) or who have atrial fibrillation with >250 bpm, or in whom the atrial fibrillation has degenerated to ventricular fibrillation, require immediate DC cardioversion.
- A 50- to 360-J biphasic synchronized DC shock can be used (commonly the initial cardioversion is attempted with 50 J for supraventricular tachycardia, but up to 360 J may be needed for cardioversion of atrial fibrillation with rapid ventricular response). DC cardioversion without the synchronized mode can induce ventricular fibrillation.
- Conscious sedation (e.g., with intravenous propofol) is also required.
stable: narrow complex (orthodromic atrioventricular reciprocating) tachycardia
carotid sinus massage or Valsalva maneuver
Comments
- Because orthodromic reciprocating tachycardia involves the atrioventricular (AV) node as one limb of the circus movement tachycardia, any maneuver or drug that slows or interrupts conduction in the AV node can terminate the tachycardia. In a hemodynamically stable patient, vagal maneuvers such as a carotid sinus massage should be performed at the bedside, or, alternatively, patients can be instructed to perform a Valsalva maneuver to terminate the arrhythmia.
intravenous adenosine or atrioventricular (AV) nodal blocking drugs or antiarrhythmics
Primary Options
- adenosine
6 mg intravenously initially, followed by 12 mg intravenously in 1-2 minutes if required
- adenosine
Secondary Options
- diltiazem
0.25 mg/kg (average adult dose 20 mg) intravenously initially, followed by 0.35 mg/kg (average adult dose 25 mg) intravenously in 15 minutes if required
- diltiazem
- verapamil
2.5 to 5 mg intravenously initially, followed by 5-10 mg (or 0.15 mg/kg) intravenously in 15-30 minutes if required, maximum 30 mg/total dose
- verapamil
- metoprolol tartrate
2.5 to 5 mg intravenously every 2-5 minutes as needed, maximum 15 mg/total dose
- metoprolol tartrate
Tertiary Options
- procainamide
100 mg intravenously every 5 minutes as needed, maximum 1000 mg/total dose
- procainamide
- ibutilide
<60 kg body-weight: 0.01 mg/kg intravenously initially, followed by 0.01 mg/kg intravenously in 10 minutes if required; ≥60 kg body-weight: 1 mg intravenously initially, followed by 1 mg intravenously in 10 minutes if required
- ibutilide
- amiodarone
150 mg intravenously initially, followed by 0.5 to 1 mg/minute intravenous infusion if needed
- amiodarone
Comments
- Adenosine is preferred because of its ultra-short half life (<18 seconds). It should be given as a rapid intravenous injection in a central vein or in the antecubital vein, followed by 10-20 mL of rapid normal saline flush. It can be used a second time if there is no response.
- Adenosine injection may cause chest pain, chest tightness, bronchospasm, dizziness, and a short run of atrial fibrillation (1% to 15%). Although atrial fibrillation is usually transient, it can cause rapid conduction to the ventricle via the accessory pathway, and if the conduction is rapid then it can potentially result in ventricular fibrillation. Therefore, resuscitation equipment should be available as a standby. Adenosine should be avoided in patients with severe asthma and patients with a known hypersensitivity to the drug. In addition, adenosine injection is associated with a higher risk of heart block in patients on carbamazepine therapy.
- AV nodal blocking drugs (diltiazem, verapamil, metoprolol) can be used when there is no response or a recurrence after carotid sinus massage and adenosine.
- Antiarrhythmic drugs (procainamide, ibutilide, amiodarone) can be used when there is no response or a recurrence after carotid sinus massage, adenosine, and AV nodal blocking drugs.
rapid atrial pacing
Comments
- Rapid atrial pacing using a temporary pacemaker for overdrive suppression of the tachycardia can be used if previous drug treatments fail.
direct-current (DC) cardioversion
Comments
- In patients whose symptoms persist despite pharmacotherapy or atrial pacing, DC cardioconversion should be used.
- A 50- to 360-J biphasic synchronized DC shock can be used (commonly the initial cardioversion is attempted with 50 J for supraventricular tachycardia, but up to 360 J may be needed for cardioversion of atrial fibrillation with rapid ventricular response). DC cardioversion without the synchronized mode can induce ventricular fibrillation.
- Conscious sedation (e.g., with intravenous propofol) is also required.
stable: wide complex (antidromic atrioventricular reciprocating) tachycardia
intravenous adenosine or antiarrhythmics
Primary Options
- adenosine
6 mg intravenously initially, followed by 12 mg intravenously in 1-2 minutes if required
- adenosine
Secondary Options
- procainamide
100 mg intravenously every 5 minutes as needed, maximum 1000 mg/total dose
- procainamide
- ibutilide
<60 kg body-weight: 0.01 mg/kg intravenously initially, followed by 0.01 mg/kg intravenously in 10 minutes if required; ≥60 kg body-weight: 1 mg intravenously initially, followed by 1 mg intravenously in 10 minutes if required
- ibutilide
- amiodarone
150 mg intravenously initially, followed by 0.5 to 1 mg/minute intravenous infusion if needed
- amiodarone
Comments
- If the tachycardia is hemodynamically stable, then management is with intravenous adenosine or antiarrhythmic drugs.
- Adenosine is preferred because of its ultra-short half life (<18 seconds). It should be given as a rapid intravenous injection in a central vein or in the antecubital vein, followed by 10-20 mL of rapid normal saline flush. It can be used a second time if there is no response.
- Adenosine injection may cause chest pain, chest tightness, bronchospasm, dizziness, and a short run of atrial fibrillation (1% to 15%). Although atrial fibrillation is usually transient, it can cause rapid conduction to the ventricle via the accessory pathway, and if the conduction is rapid then it can potentially result in ventricular fibrillation. Therefore, resuscitation equipment should be available as a standby. Adenosine should be avoided in patients with severe asthma and patients with a known hypersensitivity to the drug. In addition, adenosine injection is associated with a higher risk of heart block in patients on carbamazepine therapy.
- Antiarrhythmic drugs (procainamide, ibutilide, amiodarone) can also be used when there is no response or a recurrence after adenosine.
- Calcium-channel blockers, digoxin, and beta-blockers are contraindicated in this population, because these drugs slow the conduction via the atrioventricular node but do not have any effect on the accessory pathway. This may result in a rapid conduction via the accessory pathway, which may cause ventricular tachycardia and ventricular fibrillation leading to sudden cardiac death.
rapid atrial pacing
Comments
- Rapid atrial pacing using a temporary pacemaker for overdrive suppression of the tachycardia can be used if previous drug treatments fail.
direct-current (DC) cardioversion
Comments
- In patients whose symptoms persist despite pharmacotherapy or atrial pacing, DC cardioconversion should be used.
- A 50- to 360-J biphasic synchronized DC shock can be used (commonly the initial cardioversion is attempted with 50 J for supraventricular tachycardia, but up to 360 J may be needed for cardioversion of atrial fibrillation with rapid ventricular response). DC cardioversion without the synchronized mode can induce ventricular fibrillation.
- Conscious sedation (e.g., with intravenous propofol) is also required.
stable: pre-excited tachycardia due to atrial fibrillation or atrial flutter
antiarrhythmics + consider anticoagulation
Primary Options
- procainamide
100 mg intravenously every 5 minutes as needed, maximum 1000 mg/total dose
- procainamide
- ibutilide
<60 kg body-weight: 0.01 mg/kg intravenously initially, followed by 0.01 mg/kg intravenously in 10 minutes if required; ≥60 kg body-weight: 1 mg intravenously initially, followed by 1 mg intravenously in 10 minutes if required
- ibutilide
Comments
- Pre-excited tachycardia results in a rapid irregular wide complex tachycardia with varying duration and amplitude of QRS complexes depending upon the degree of pre-excitation.
- Anticoagulation should be considered in atrial fibrillation and atrial flutter depending on presence of comorbid cardiologic abnormalities and duration of onset.
rapid atrial pacing (for atrial flutter)
Comments
- In atrial flutter, rapid atrial pacing using a temporary pacemaker for overdrive suppression of the atrial flutter can be used if the previous drug treatments fail.
- Rapid atrial pacing has no role in atrial fibrillation.
direct-current (DC) cardioversion
Comments
- In patients with atrial fibrillation or atrial flutter whose symptoms persist despite antiarrhythmic agents, DC cardioconversion should be used.
- A 50- to 360-J biphasic synchronized DC shock can be used (commonly the initial cardioversion is attempted with 50 J for supraventricular tachycardia, but up to 360 J may be needed for cardioversion of atrial fibrillation with rapid ventricular response). DC cardioversion without the synchronized mode can induce ventricular fibrillation.
- Conscious sedation (e.g., with intravenous propofol) is also required.
stable: pre-excited tachycardia due to atrial tachycardia
antiarrhythmics
Primary Options
- procainamide
100 mg intravenously every 5 minutes as needed, maximum 1000 mg/total dose
- procainamide
- ibutilide
<60 kg body-weight: 0.01 mg/kg intravenously initially, followed by 0.01 mg/kg intravenously in 10 minutes if required; ≥60 kg body-weight: 1 mg intravenously initially, followed by 1 mg intravenously in 10 minutes if required
- ibutilide
- amiodarone
150 mg intravenously initially, followed by 0.5 to 1 mg/minute intravenous infusion if needed
- amiodarone
Comments
- Pre-excited tachycardia results in a rapid irregular wide complex tachycardia with varying duration and amplitude of QRS complexes depending upon the degree of pre-excitation.
rapid atrial pacing
Comments
- Rapid atrial pacing using a temporary pacemaker for overdrive suppression of the atrial tachycardia can be used if previous drug treatments fail.
direct-current (DC) cardioversion
Comments
- In patients with atrial tachycardia whose symptoms persist despite antiarrhythmic agents or atrial pacing, DC cardioconversion should be used.
- A 50- to 360-J biphasic synchronized DC shock can be used (commonly the initial cardioversion is attempted with 50 J for supraventricular tachycardia, but up to 360 J may be needed for cardioversion of atrial fibrillation with rapid ventricular response). DC cardioversion without the synchronized mode can induce ventricular fibrillation.
- Conscious sedation (e.g., with intravenous propofol) is also required.
- However, the recurrence of atrial arrhythmia after DC cardioversion may be higher in atrial tachycardia, compared with atrial fibrillation/flutter, depending on the mechanism. If the atrial tachycardia is related to abnormal automaticity, DC cardioversion may not be effective at all, such as in multifocal atrial tachycardia.
following acute treatment: asymptomatic
catheter ablation
Comments
- Asymptomatic patients in specialized jobs with particular safety issues (e.g., airline pilot, school bus driver) can be considered for catheter ablation. Catheter ablation is also performed in asymptomatic patients who are found to have a "high-risk" accessory pathway at the time of electrophysiology testing, showing high-risk antegrade conduction characteristics.[3] [20]
- Catheter ablation is generally not performed in pregnant patients and should be deferred until after delivery.
following acute treatment: symptomatic
catheter ablation
Comments
- All patients should be offered catheter ablation.
- The incidence of symptomatic tachycardia is reported to be higher during pregnancy, which may be refractory to drugs that are safe to use in such circumstances. Therefore a radiofrequency ablation should be considered prior to the next planned pregnancy. Catheter ablation is generally not performed in pregnant patients and should be deferred until after delivery.
antiarrhythmics
Primary Options
- flecainide
50-150 mg orally twice daily
- flecainide
- propafenone
150-300 mg orally (immediate-release) every 8 hours
- propafenone
- sotalol
80-160 mg orally twice daily
- sotalol
- 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
- amiodarone
- dofetilide
125-500 micrograms orally twice daily
- dofetilide
Comments
- Used in patients who refuse ablation or in whom ablation is unsuitable.
- Class I antiarrhythmic agents (flecainide or propafenone) are suitable for patients with no additional cardiac disease but cannot be used in people with coronary artery disease or structural heart disease.
- In patients with coronary artery disease or structural heart disease, class III antiarrhythmic agents (sotalol, amiodarone, or dofetilide) may be used.
- In the event a patient with WPW syndrome becomes pregnant prior to ablation of their accessory pathway, and if frequent recurrences of SVT are observed during pregnancy, it is reasonable to treat the patients with flecainide or propafenone.[3]
- QT interval must be determined prior to starting therapy with dofetilide as it is contraindicated if QTc is >440 msec (>500 msec in patients with ventricular conduction abnormalities).
Follow-Up Overview
Prognosis
Monitoring
Complications
Citations
Brugada J, Katritsis DG, Arbelo E, et al. 2019 ESC Guidelines for the management of patients with supraventricular tachycardia. The Task Force for the management of patients with supraventricular tachycardia of the European Society of Cardiology (ESC). Eur Heart J. 2020 Feb 1;41(5):655-720.[Abstract][Full Text]
Zeppenfeld K, Tfelt-Hansen J, de Riva M, et al. 2022 ESC Guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death. Eur Heart J. 2022 Oct 21;43(40):3997-4126.[Abstract][Full Text]
Page RL, Joglar JA, Caldwell MA, et al. 2015 ACC/AHA/HRS guideline for the management of adult patients with supraventricular tachycardia: a report of the American College of Cardiology/American Heart Association Task Force on Clinical Practice Guidelines and the Heart Rhythm Society. J Am Coll Cardiol. 2016 Apr 5;67(13):e27-115.[Abstract][Full Text]
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16. Cohen MI, Triedman JK, Cannon BC, et al. PACES/HRS expert consensus statement on the management of the asymptomatic young patient with a Wolff-Parkinson-White (WPW, ventricular preexcitation) electrocardiographic pattern: developed in partnership between the Pediatric and Congenital Electrophysiology Society (PACES) and the Heart Rhythm Society (HRS). Heart Rhythm. 2012 Jun;9(6):1006-24.[Abstract][Full Text]
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Key Articles
Referenced Articles
Guidelines
Diagnostic
Summary
Provides clinical practice guidelines on the evaluation and management of asymptomatic young patients (from 8-21 years of age) with a WPW electrocardiographic pattern. Following a formal literature review, members from PACES and HRS weighed the strength of the evidence for or against an observational strategy or a particular procedure in evaluation and management of asymptomatic patients with WPW.Published by
Pediatric and Congenital Electrophysiology Society; Heart Rhythm Society
Published
2012
Treatment
Summary
Comprehensive recommendations on the treatment of patients who have or may be at risk for ventricular arrhythmias. Includes therapies, the role of drugs, implantable devices, and ablation in acute and chronic management. The guidelines attempt to individualize prognosis and management according to symptom burden and severity of underlying heart disease in addition to clinical presentation.Published by
American College of Cardiology; American Heart Association Task Force on Clinical Practice Guidelines; Heart Rhythm Society
Published
2017
Summary
Guideline for the management of adults with all types of supraventricular tachycardia (other than atrial fibrillation).Published by
American College of Cardiology; American Heart Association Task Force on Clinical Practice Guidelines; Heart Rhythm Society
Published
2015
Summary
Evidence-based guidelines on the management of atrial fibrillation, with special considerations for WPW syndrome.Published by
American College of Cardiology; American Heart Association Task Force on Clinical Practice Guidelines; Heart Rhythm Society
Published
2014
Summary
Provides clinical practice guidelines on the evaluation and management of asymptomatic young patients (from 8-21 years of age) with a WPW electrocardiographic pattern. Following a formal literature review, members from PACES and HRS weighed the strength of the evidence for or against an observational strategy or a particular procedure in evaluation and management of asymptomatic patients with WPW.Published by
Pediatric and Congenital Electrophysiology Society; Heart Rhythm Society
Published
2012
Summary
European guidelines for the management of patients with ventricular arrhythmias and the prevention of sudden cardiac death, including new evidence on genetics and risk stratification, as well as therapeutic strategies.Published by
European Society of Cardiology
Published
2022
Summary
Updated evidence-based guidelines on the management of atrial fibrillation.Published by
European Society of Cardiology
Published
2020