Treatment of arrhythmias associated with the Wolff-Parkinson-White syndrome

INTRODUCTION — 

Patients with the Wolff-Parkinson-White (WPW) syndrome have an accessory pathway that directly connects the atria and ventricles, allowing conduction to bypass the atrioventricular (AV) node. When there is conduction over an accessory pathway, the ventricles are activated earlier than if the impulse had traveled through the AV node. This early activation, referred to as preexcitation, is responsible for the classic electrocardiographic (ECG) findings of a shortened PR interval and, in most patients, a delta wave (waveform 1). Patients with evidence of preexcitation on ECG are said to have WPW pattern, while those who develop arrhythmias involving the accessory pathway have WPW syndrome.

This topic will review the available therapeutic options for the treatment and prevention of arrhythmias in WPW syndrome. The clinical manifestations and approach to diagnosis are discussed separately. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis" and "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway".)

ACUTE MANAGEMENT OF ARRHYTHMIAS — 

Patients with Wolff-Parkinson-White (WPW) may present with acute tachyarrhythmias. There are three major arrhythmias that occur in these patients: orthodromic atrioventricular reentrant tachycardia (AVRT), antidromic AVRT, and atrial fibrillation (AF). All three arrhythmias typically cause symptoms (eg, palpitations, dizziness), while AF may potentially cause ventricular fibrillation (VF) and sudden cardiac death. For these reasons, patients who present with an acute arrhythmia require pharmacologic therapy for restoration of sinus rhythm. However, because of the electrophysiologic differences between AV nodal tissue and the tissue comprising an accessory pathway, standard therapy for heart rate control may worsen symptoms and lead to clinical deterioration in these patients. Our approach to treating acute tachyarrhythmias in patients with a known or suspected accessory pathway is discussed below. Patients should be managed in a carefully monitored environment such as an emergency department, with intravenous (IV) access established and equipment on hand for electrical cardioversion or defibrillation if needed.

Unstable patients — Patients are considered to be unstable if they have hypotension, altered mental status, chest pain, or acute heart failure. Unstable patients should undergo urgent electrical cardioversion [1,2]. The technique for urgent electrical cardioversion is discussed elsewhere. (See "Cardioversion for specific arrhythmias".)

Stable patients — If a patient is hemodynamically stable (ie, does not have hypotension, altered mental status, chest discomfort, or acute heart failure), we evaluate the 12-lead electrocardiogram (ECG) to determine the type of arrhythmia present.

Orthodromic AVRT (regular, narrow QRS complex) — If the arrhythmia appears regular and the QRS complex is narrow, the most likely diagnosis is orthodromic AVRT (waveform 2). In this arrhythmia, antegrade conduction occurs via the AV node with retrograde conduction via an accessory pathway. In such patients, antegrade conduction via the AV node is typically the "weak link" of the reentrant circuit, meaning that therapy directed at lengthening AV nodal refractoriness should terminate the arrhythmia. Thus, the initial approach to patients with orthodromic AVRT is similar to the approach taken with patients who have other types of paroxysmal supraventricular tachycardia (eg, AV nodal reentrant tachycardia). (See "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway", section on 'Narrow complex AVRT' and "Overview of the acute management of tachyarrhythmias", section on 'Regular narrow QRS complex tachyarrhythmias'.)

We employ a sequential approach to the termination of orthodromic AVRT (table 1):

●Vagal maneuvers – We first perform one or more vagal maneuvers (eg, Valsalva maneuver, carotid sinus massage) [1,2]. In many cases, vagal maneuvers are sufficient to terminate the arrhythmia [3]. (See "Vagal maneuvers".)

●Adenosine – If vagal maneuvers are ineffective, we suggest IV adenosine rather than other AV nodal-blocking agents (eg, verapamil) based on its efficacy, safety, and rapid onset of effect. The protocol for IV adenosine administration is described in the algorithm (algorithm 1). IV adenosine is effective for acute termination of orthodromic AVRT in 80 to 90 percent of patients [4-6]. On rare occasions, adenosine has been reported to increase the vulnerability of the atria to AF transiently, a potentially serious proarrhythmic effect. Adenosine may also cause atrial ectopy that may reinitiate orthodromic AVRT after acute tachycardia termination [4,7-9].

●Verapamil or diltiazem – If adenosine is ineffective, we administer an IV nondihydropyridine calcium channel blocker (eg, verapamil, diltiazem), assuming the patient does not have hypotension or reduced left ventricular systolic function. We typically choose IV verapamil, given as 5 mg boluses in a fully-grown patient (0.1 mg/kg in children to a maximum dose of 5 mg; contraindicated in children less than 12 months of age) every two to three minutes (up to a cumulative initial dose of up to 15 mg). While verapamil is as effective as adenosine for acutely terminating orthodromic AVRT, it has a longer half-life and may be less effective. (table 1) [10,11]. (See "Calcium channel blockers in the treatment of cardiac arrhythmias".)

●Procainamide or beta blocker – If vagal maneuvers, adenosine, and verapamil are ineffective in terminating orthodromic AVRT, therapeutic options include IV procainamide or an IV beta blocker (eg, propranolol, metoprolol, esmolol) [12-14]. We reserve these drugs for patients with arrhythmias that have proven refractory to vagal maneuvers, adenosine, and verapamil because they are less effective and (in the case of procainamide) require an infusion rather than a bolus administration.

•Procainamide slows conduction and prolongs refractoriness in atrial and ventricular myocardium, accessory pathways, and the His-Purkinje system, while causing slight shortening of (or no effect on) the AV nodal refractory period [15,16]. An approach to procainamide infusion in adults is described in the algorithm (algorithm 2). For young children, the dose for procainamide is a bolus given over 15 to 30 minutes (7 to 10 mg/kg bolus for infants <12 months of age compared with 10 to 15 mg/kg bolus for children older than 12 months), followed by an infusion of 20 to 50 micrograms/kg/minute.

•Beta blockers decrease conduction through the AV node and do not impact the refractory period of the accessory pathway. We typically use metoprolol, which is administered as a 2.5 to 5 mg IV bolus over two to five minutes; if there is no response, we give an additional 2.5 to 5 mg IV bolus every 10 minutes to a total dose of 15 mg.

A regular, narrow QRS complex tachycardia that fails to terminate with the above therapies may be an arrhythmia other than orthodromic AVRT (eg, atrial flutter); if we suspect atrial flutter, we manage the patient in a similar manner to a patient with AF (see 'Atrial fibrillation with preexcitation (irregular, wide QRS complex)' below). Alternatively, if the patient is a child, the rhythm may be permanent junctional reciprocating tachycardia (PJRT), which is a rare, persistent form of orthodromic AVRT with a long RP interval on the surface ECG that usually occurs in early childhood. PJRT involves a slowly conducting concealed accessory pathway that is usually posteroseptal in location. Catheter ablation is the preferred treatment [17]. PJRT is discussed in detail elsewhere. (See "Atrioventricular reentrant tachycardia (AVRT) associated with an accessory pathway", section on 'Permanent junctional reciprocating tachycardia'.)

After termination of the acute arrhythmia, we take steps to prevent recurrence. (See 'Prevention of recurrent arrhythmias' below.)

Antidromic AVRT (regular, wide QRS complex) — If the arrhythmia appears regular and the QRS complex is wide, the most likely diagnosis is antidromic AVRT (waveform 3). In this arrhythmia, antegrade conduction occurs via the accessory pathway. Retrograde conduction is usually via the AV node but may be via a second accessory pathway if multiple pathways are present. Our approach to treating the arrhythmia depends on our certainty that the wide QRS complex tachycardia is antidromic AVRT as opposed to another arrhythmia (eg, ventricular tachycardia) [2]. As an example, we would strongly suspect antidromic AVRT in a young patient who is known to have WPW, but the diagnosis would be less certain in a middle-aged patient with both WPW and risk factors for coronary artery disease (CAD).

●When the diagnosis is uncertain – If the diagnosis of antidromic AVRT is uncertain, the arrhythmia should be treated as an undiagnosed wide QRS tachycardia. (See "Wide QRS complex tachycardias: Approach to the diagnosis" and "Wide QRS complex tachycardias: Approach to management".)

●When antidromic AVRT is certain or nearly certain – If the patient has WPW and a low risk of CAD, it is reasonable to use the following sequential approach for the treatment of antidromic AVRT:

•Vagal maneuvers – We first perform one or more vagal maneuvers (eg, Valsalva maneuver, carotid sinus massage) [1,2]. These may be sufficient to terminate the arrhythmia [3]. (See "Vagal maneuvers".)

•Procainamide – If vagal maneuvers fail to terminate the arrhythmia, we recommend procainamide. Procainamide slows conduction and prolongs refractoriness in the accessory pathway. Dosing of procainamide can be found in the algorithm (algorithm 2).

•Consider reasons for persistent arrhythmia – Failure of vagal maneuvers, adenosine, and procainamide to terminate the arrhythmia suggests two possibilities:

-The rhythm is a different arrhythmia (eg, atrial flutter with preexcitation, ventricular tachycardia), not antidromic AVRT.

-The rhythm is antidromic AVRT with a circuit that involves two accessory pathways rather than one accessory pathway and the AV node.

Electrophysiology study (EPS) may be required to discover the reason for the persistent arrhythmia and determine the most appropriate treatment.

Verapamil, diltiazem, and beta blockers are contraindicated for the acute management of antidromic AVRT because there is a risk that the drug will increase the rate of the arrhythmia, potentially causing hemodynamic instability and even ventricular fibrillation (VF). Verapamil carries this risk because it may indirectly reduce the refractoriness of the accessory pathway due to a reflex increase in sympathetic tone, which is brought on by a reduction in myocardial contractility and systemic vascular resistance.

After termination of the acute arrhythmia, we take steps to prevent recurrence. (See 'Prevention of recurrent arrhythmias' below.)

Atrial fibrillation with preexcitation (irregular, wide QRS complex) — In patients with an accessory pathway capable of antegrade conduction who develop AF, conduction to the ventricle often occurs through a combination of the normal conduction pathway (via the AV node) and the accessory pathway. However, because most accessory pathways have a shorter refractory period than the AV node, the ventricular rate can be more rapid if AV conduction occurs preferentially via the accessory pathway. The ECG in preexcited AF typically reveals irregular ventricular activity, high ventricular rates (often >200 bpm), wide QRS complexes, and beat-to-beat variation in QRS width; unlike polymorphic ventricular tachycardia, the axis remains stable (waveform 4).

Our approach to the acute treatment of patients with AF with preexcitation (also known as “preexcited AF”) is consistent with published professional society guidelines [1,2,18].

●We recommend terminating the arrhythmia using an IV antiarrhythmic such as procainamide or ibutilide that lengthens antegrade refractoriness and slows conduction in both the AV node/His-Purkinje system and the accessory pathway [1,2]. It is important to note that all AV nodal-blocking agents (eg, adenosine, beta blockers, verapamil, diltiazem, digoxin, sotalol, and amiodarone) are contraindicated for patients with preexcited AF because blocking the AV node will promote conduction down the accessory pathway and in some cases may directly enhance the rate of conduction over the accessory pathway; these effects may increase the ventricular rate, which may cause hemodynamic instability and degeneration of the rhythm into VF [18-21].

•IV procainamide (algorithm 2) is effective for acute therapy of preexcited AF because of its effects on atrial and ventricular myocardium without any AV nodal-blocking effect. Procainamide is usually the preferred IV drug option for preexcited AF in children. For young children, the dose for procainamide is a bolus given over 15 to 30 minutes (7 to 10 mg/kg bolus for infants <12 months of age compared with 10 to 15 mg/kg bolus for children older than 12 months), followed by an infusion of 20 to 50 micrograms/kg/minute. If AF persists despite procainamide, the ventricular rate is usually slower due to effects on refractoriness and conduction in the accessory pathway.

•Ibutilide, a class III antiarrhythmic drug that prolongs the refractoriness of the AV node, His-Purkinje system, and accessory pathway, is useful for acute termination of AF. In one series of 22 patients with WPW and AF during an EPS, ibutilide prolonged the shortest preexcited R-R interval and terminated the arrhythmia in 95 percent [22]. The pediatric experience with ibutilide is very limited. (See "Therapeutic use of ibutilide".)

•The class IC antiarrhythmic drugs (eg, flecainide, propafenone) and the class III agent dofetilide are effective when used in this setting, but the parenteral formulations of these drugs are not approved for use in some countries, including the United States.

After termination of the acute arrhythmia, we take steps to prevent recurrence. (See 'Prevention of recurrent arrhythmias' below.)

PREVENTION OF RECURRENT ARRHYTHMIAS — 

After termination of an acute tachyarrhythmia, patients with Wolff-Parkinson-White (WPW) syndrome should be evaluated for additional therapy aimed at preventing recurrent symptomatic arrhythmias.

Catheter ablation as initial therapy

Efficacy and safety — We suggest catheter ablation rather than pharmacologic therapy due to the efficacy and safety of ablation (waveform 5) [1]. Therapy with antiarrhythmic medications is less likely to prevent arrhythmias and exposes the patient to potential adverse effects.

Numerous studies have confirmed that catheter ablation of accessory pathways is safe and effective [23-29]. The short-term success rate with catheter ablation is approximately 85 to 95 percent but varies depending on the location of the accessory pathway, the number of pathways, and the depth of the pathway within the myocardium (ie, epicardial versus endocardial) (waveform 6 and waveform 7) [23,24,26-35]. Long-term success rates may be closer to 80 percent at five years postablation [36]. Recurrent arrhythmias involving an accessory pathway have been reported in 5 to 12 percent of patients who undergo catheter ablation for WPW syndrome [28,31,32,37,38]. The recurrence rate is higher with ablation of septal accessory pathways or multiple pathways [33,37,38]. Approximately one-half of recurrences occur in the first 12 hours after the procedure [38].

Data on complication rates come from both case series and a voluntary national registry. The reported incidence of nonfatal complications is on the order of 2 to 4 percent, which is similar to rates seen with ablation procedures for other arrhythmias [27,28,39]. In a registry that included 654 patients with WPW syndrome who underwent ablation, major procedural complications occurred in 2 percent; the most common complication was cardiac tamponade. Specific complications that are related to the anatomic site of ablation, including complete atrioventricular (AV) block resulting from ablation of a septal accessory pathway near the AV node, acute interatrial shunting related to transseptal catheterization for ablation of left-sided accessory pathways (although there are usually no adverse long-term sequelae), and inappropriate sinus tachycardia, may be present following ablation of a posteroseptal accessory pathway, suggesting disruption of the parasympathetic and/or sympathetic innervation of the sinus and AV nodes [40-46]. (See "Overview of catheter ablation of cardiac arrhythmias", section on 'Complications'.)

Technical aspects — The standard energy source used to ablate accessory pathways is radiofrequency current, although cryoenergy can be used as an alternative to radiofrequency energy to ablate accessory pathways that are in close proximity to the AV node or bundle of His [47]. In a meta-analysis that included data from 64 studies, including 3495 patients undergoing radiofrequency catheter ablation (RFA) and 749 patients undergoing cryoablation of septal accessory pathways, acute procedural success was similar with either approach (89 versus 86 percent with RFA versus cryoablation, respectively) [35]. Long-term success rates were higher with RFA (88 versus 76 percent with cryoablation), although cryoablation resulted in lower risk of persistent AV block (0 versus 3 percent with RFA).

The location of most accessory pathways can be estimated using the preexcitation pattern on the surface electrocardiogram (ECG). However, more precise localization of the accessory pathway during catheter-based mapping prior to catheter ablation utilizes several parameters [26].

●Atrial insertion site – To determine the atrial insertion site, the earliest site of retrograde atrial activation during orthodromic AV reentrant tachycardia (AVRT) or ventricular pacing must be identified [48,49]. The assumption is that the local retrograde ventriculoatrial (VA) interval on the recording electrode will be shortest at the atrial insertion site. Compared with pacing at sites more remote from the accessory pathway, atrial pacing near the atrial insertion of the accessory pathway will create a greater degree of preexcitation with a shorter delay between the stimulus and the onset of the delta wave [50].

●Ventricular insertion site – More precise localization of the ventricular insertion site is obtained by mapping along the AV groove in sinus rhythm to determine the site of earliest ventricular activation during preexcited beats. Local ventricular activation at the ventricular insertion site frequently precedes the onset of the delta wave on the surface ECG by 10 to 40 milliseconds (waveform 8) [51,52]. If preexcitation is minimal in sinus rhythm, then atrial pacing can be performed to facilitate ventricular preexcitation by delaying AV nodal conduction.

●Multiple accessory pathways – Multiple accessory pathways are found in as many as 13 percent of patients with WPW syndrome. Ablation of multiple accessory pathways is possible, but it requires a longer procedure time and is associated with a higher rate of recurrence [27,37,53]. As an example, in one study of 858 patients undergoing electrophysiology study (ESP) and ablation for WPW syndrome in which multiple accessory pathways were identified in 8.5 percent of patients, procedural success was similar for single and multiple pathways, but the rate of recurrent arrhythmias over a mean follow-up of 43 months was higher in persons with multiple accessory pathways (9.5 versus 2.5 percent) [37].

●Epicardial accessory pathway location – Successful catheter ablation is more challenging when the accessory pathway is located close to the epicardial surface than when it is endocardial. In patients with epicardial pathways, the usual ablation procedure via transvenous catheters at the endocardial surface may not affect the critical tissue. Although not widely done, percutaneous epicardial ablation is possible via subxiphoid access of the pericardial space. The feasibility of this approach was demonstrated in a report of 48 patients with a variety of arrhythmias (10 with WPW syndrome) who had failed endocardial ablation [54]. Via subxiphoid instrumentation, 5 of the 10 patients had accessory pathways localized to the epicardial surface, and three were successfully ablated.

To unmask any residual conduction via an accessory pathway prior to ending the ablation procedure, intravenous (IV) adenosine can be administered to transiently block the AV node. We primarily use adenosine when it is difficult to determine if the pathway has been successfully ablated.

Alternative therapy

Antiarrhythmic drugs — For patients who are not candidates for catheter ablation or do not wish to undergo the procedure, we initiate antiarrhythmic therapy [1]. The pharmacologic agents discussed below are appropriate both for patients who have had AVRT and for those who have had preexcited atrial fibrillation (AF) unless otherwise specified (table 1).

●For patients without coronary artery disease (CAD), we typically choose a class IC antiarrhythmic drug (eg, flecainide, propafenone) (table 2) because these drugs are effective at preventing AVRT [55-58] and atrial fibrillation (AF) [59,60]. We generally choose propafenone because it has mild beta-blocking activity in addition to its other effects [57,58]. We initiate propafenone immediate release 150 mg every 8 hours or propafenone extended release 225 mg every 12 hours.

●For patients who have CAD, we do not use class IC agents because these drugs may increase mortality by causing arrhythmias [61]. We typically use a class III agent (eg, amiodarone, dofetilide) for the prevention of arrhythmias in these patients. When choosing between the class III agents, we consider the patient’s age, underlying comorbidities, and the nature of their clinical presentation during the arrhythmia (eg, hemodynamic stability, severity of symptoms).

Amiodarone, in particular, has multiple electrophysiologic effects that make it effective, including beta-blocking activity, class III effects to prolong action potential repolarization, blockade of the fast sodium and slow calcium inward currents, and suppression of ectopic beats [62-66]. These effects result in the slowing of impulse conduction and lengthening of refractoriness in both the bypass tract and the AV node/His-Purkinje system. However, amiodarone has several common adverse effects, including pulmonary, thyroid, and hepatic toxicity, which is a concern for patients with WPW syndrome who are often young and may require many years of therapy. Dosing and side effects of amiodarone and dofetilide are discussed elsewhere. (See "Amiodarone: Adverse effects, potential toxicities, and approach to monitoring" and "Amiodarone: Clinical uses", section on 'Oral amiodarone for the treatment of atrial arrhythmias' and "Clinical use of dofetilide".)

Unlike IV amiodarone, oral amiodarone is not contraindicated for patients with WPW syndrome [67,68]. IV and oral amiodarone have different effects on accessory pathway conduction; while IV amiodarone does not seem to impact accessory pathway conduction, chronic oral amiodarone may slow conduction in an accessory pathway.

●For patients with a history of AVRT but not AF, beta blockers may be reasonable if the accessory pathway appears to be "low-risk" (eg, only intermittently manifest or known to have a long effective refractory period). Beta blockers do not change accessory pathway refractoriness. However, for patients who are in preexcited AF, slowing of AV nodal conduction may decrease the degree of concealed retrograde conduction into the accessory pathway, allowing for increased antegrade conduction through the pathway and increasing the risk of ventricular fibrillation (VF).

●Verapamil, diltiazem, and digoxin are contraindicated as chronic therapy for patients with WPW syndrome. Verapamil may indirectly reduce the refractoriness of the accessory pathway due to a reflex increase in sympathetic tone brought on by a reduction in myocardial contractility and systemic vascular resistance. Digoxin slows AV nodal conduction by a vasomimetic mechanism, has an unpredictable effect on accessory pathway refractoriness [69], and reduces concealed retrograde conduction into the accessory. If a patient with WPW syndrome who is taking verapamil or digoxin develops AF or antidromic AVRT, rapid conduction down the accessory pathway could lead to hemodynamic deterioration and even VF.

Therapy for recurrence

Repeat catheter ablation and surgical ablation — For patients who have undergone ablation and present with recurrent tachyarrhythmias and the return of delta waves on the ECG, we perform an EPS. If the EPS reveals conduction through an accessory pathway, repeat catheter ablation is indicated. Repeat ablation usually leads to a permanent cure in patients who experience a recurrence [38].

If repeat catheter ablation is unsuccessful, surgical ablation may be appropriate. The long-term success rate for WPW surgery is almost 100 percent, with an operative mortality rate of less than 1 percent [70-72]; however, surgical ablation is more invasive and requires a longer recovery time. Surgical ablation should be performed at centers with a proven track record of success in performing the procedure [73].

RISK STRATIFICATION OF PATIENTS WITHOUT ARRHYTHMIAS — 

Some patients who have Wolff-Parkinson-White (WPW) pattern on their electrocardiogram (ECG) and have never had an arrhythmia benefit from treatment (eg, catheter ablation) because they are at risk of developing hemodynamically significant arrhythmias and sudden cardiac death [30]. Risk stratification with exercise ECG testing is appropriate for certain asymptomatic patients. Our approach to the risk stratification of asymptomatic patients is discussed in detail elsewhere. (algorithm 3). (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Risk stratification of asymptomatic patients with WPW pattern'.)

SOCIETY GUIDELINE LINKS — 

Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Atrial fibrillation" and "Society guideline links: Arrhythmias in adults" and "Society guideline links: Catheter ablation of arrhythmias" and "Society guideline links: Supraventricular arrhythmias".)

INFORMATION FOR PATIENTS — 

UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5^th to 6^th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10^th to 12^th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.

Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)

●Basics topic (see "Patient education: Wolff-Parkinson-White syndrome (The Basics)")

●Beyond the Basics topic (see "Patient education: Wolff-Parkinson-White syndrome (Beyond the Basics)")

SUMMARY AND RECOMMENDATIONS

●Introduction – Patients with Wolff-Parkinson-White (WPW) syndrome experience three types of arrhythmias that involve an accessory pathway: orthodromic atrioventricular reentrant tachycardia (AVRT), antidromic AVRT, and atrial fibrillation (AF) with preexcitation.

●Acute management – Unstable patients should undergo urgent electrical cardioversion. The management of stable patients depends on the type of arrhythmia.

●Orthodromic AVRT (regular, narrow QRS complex) – For patients with orthodromic AVRT, we use the following sequential approach to arrhythmia termination: vagal maneuvers, adenosine, verapamil, and, if these approaches have not been effective, either procainamide or a beta blocker. (See 'Orthodromic AVRT (regular, narrow QRS complex)' above.)

•Antidromic AVRT (regular, wide QRS complex) – If the diagnosis of antidromic AVRT is uncertain, we treat the arrhythmia as an undiagnosed wide complex tachycardia. (See "Wide QRS complex tachycardias: Approach to management".)

If the diagnosis is certain, we use the following sequential approach: vagal maneuvers, procainamide. (See 'Antidromic AVRT (regular, wide QRS complex)' above.)

•AF with preexcitation (irregular, wide QRS complex) – For patients with preexcited AF, we use procainamide or ibutilide for arrhythmia termination. All AV nodal-blocking agents (eg, adenosine, beta blockers, calcium channel blockers, digoxin, sotalol, amiodarone) are contraindicated. (See 'Atrial fibrillation with preexcitation (irregular, wide QRS complex)' above.)

●Prevention of recurrent arrhythmias

•Initial therapy – We suggest catheter ablation rather than pharmacologic therapy for the prevention of recurrent arrhythmias (Grade 2C). The efficacy of ablation varies depending on the location, number, and depth of the pathways within the myocardium. (See 'Catheter ablation as initial therapy' above.)

•Alternative therapy – For patients who are not candidates for catheter ablation, or do not wish to undergo the procedure, we initiate antiarrhythmic therapy as follows:

-For patients without coronary artery disease (CAD), we typically choose a class IC antiarrhythmic drug (eg, flecainide, propafenone).

-For patients with CAD, we choose a class III agent (eg, amiodarone, dofetilide).

-For patients with AVRT, beta blockers may be a reasonable alternative if the accessory pathway appears to be “low risk”. We consider low risk to be those that only intermittently manifest or are known to have a long effective refractory period. Beta blockers (and all other AV nodal-blocking agents) are contraindicated for patients with a history of AF. (See 'Alternative therapy' above.)

•Therapy for recurrence – For patients who have undergone catheter ablation and present with recurrent arrhythmias, we perform an electrophysiology study (EPS) and repeat catheter ablation. If catheter ablation is unsuccessful, surgical ablation may be appropriate. (See 'Therapy for recurrence' above.)

●Risk stratification of patients without arrhythmias – For certain patients with WPW pattern who have never had an arrhythmia, we perform risk stratification with exercise electrocardiography (ECG) testing. Risk stratification is discussed elsewhere. (See "Wolff-Parkinson-White syndrome: Anatomy, epidemiology, clinical manifestations, and diagnosis", section on 'Risk stratification of asymptomatic patients with WPW pattern'.)