eMedicine Specialties > Cardiology > Arrhythmias

Wolff-Parkinson-White Syndrome: Treatment & Medication

Author: Vibhuti N Singh, MD, MPH, FACC, FSCAI, Director, Suncoast Cardiovascular Center; Chair, Cardiology Division and Cath Labs, Department of Medicine, Bayfront Medical Center; Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine
Coauthor(s): Rakesh K Sharma, MD, FACC, Adjunct Associate Professor of Medicine and Cardiology; University of Arkansas for Medical Sciences, Medical Center of South Arkansas
Contributor Information and Disclosures

Updated: Aug 24, 2009

Treatment

Medical Care

Treatment of arrhythmia is directed at the underlying cause and the triggers that perpetuate the arrhythmia. The underlying cause includes primary arrhythmias due to an EP abnormality resulting from definable structural heart disease and occurring independently of hemodynamic or metabolic disturbance. Such arrhythmias include coronary heart disease, ischemia, cardiomyopathy, pericarditis, and WPW syndrome. The triggers that perpetuate the arrhythmia include secondary arrhythmias, such as electrolyte imbalance, metabolic defects, and hemodynamic and hypoxemic abnormalities.

Appropriate treatment of WPW syndrome is based on its likely prognosis. Patients with only ECG evidence of preexcitation, without documented episodes of tachyarrhythmias, generally do not require either aggressive workup through EP studies or treatment with antiarrhythmic agents.

The 3 main treatment modalities for WPW syndrome are drug therapy, electrical (ie, RF) ablation, and surgical ablation. Ablation is the first-line treatment for symptomatic WPW syndrome. It has replaced surgical treatment and most drug treatment. However, drug therapy can be useful in some instances, such as in patients who refuse ablation, in temporizing or longer term therapy in patients with a higher risk of ablation-related complications (eg, AV block with pacing requirement for septal pathways), or in patients in whom ablation fails in 1 or 2 attempts. For patients treated longitudinally with pharmacotherapy, consideration should be given to a membrane-active antiarrhythmic drug (class IC or III) with an AV nodal blocker, rather than just an AV nodal blocker, because of the potential for extremely rapid rates during preexcited atrial fibrillation or flutter.

  • Drug therapy (potential antiarrhythmic mechanisms): Antiarrhythmic drugs act on the AV node (ie, AV node blocking agents), myocardial tissue, and/or the accessory pathways. They work by increasing the refractory period or by prolonging the conduction time to prevent perpetuation of an AV reciprocating tachycardia. They may also act to reduce the ventricular response to atrial flutter or atrial fibrillation.
    • AV node blocking drugs
      • Adenosine, verapamil, metoprolol, and digitalis all prolong conduction time and refractoriness in the AV node.
      • Verapamil and metoprolol do not affect conduction in the bypass tract.
      • Digitalis exhibits variable effects and may even shorten the refractory period.
      • None of these drugs should be given in an acute phase to a patient with ventricular preexcitation who has atrial fibrillation.
      • Digoxin is contraindicated in patients with WPW syndrome, although it may play some role in children only. Most deaths from WPW syndrome have been associated with digoxin use.
      • Metoprolol or atenolol can be useful in some patients.
    • Agents affecting the accessory pathways
      • Class IA drugs (eg, procainamide) and class IC drugs (eg, flecainide, propafenone) block conduction in the accessory pathway.
      • Amiodarone and sotalol influence both the AV node and the bypass tract. They work in similar fashion but affect only the bypass tract.
      • Class IA and IC drugs that prolong the refractory period in the bypass tract are indicated if drug therapy becomes necessary.
      • Class IC and IA drugs are best used in conjunction with an AV node blocker, such as metoprolol or verapamil.
      • Procainamide and quinidine are relics of the past for long-term treatment.
    • Caution when treating WPW syndrome tachycardia
      • Digitalis shortens refractoriness in the myocardium and in the bypass tract. Thus, it may accelerate the ventricular response in the setting of atrial fibrillation in a patient with WPW syndrome. Adenosine should not be used in this setting.
      • Digitalis should not be used in such patients, except perhaps in pediatric or elderly patients. Instead, medicines that prolong the refractory period in the accessory pathway (eg, class IA and IC agents) should be used.
      • Intravenous verapamil can likewise speed up the ventricular response in patients with WPW syndrome who have atrial fibrillation. This does not appear to happen with oral verapamil. Verapamil is not recommended as a sole agent in patients with WPW syndrome.
  • Termination of an acute episode
    • Narrow-complex AV reentrant tachycardia
      • Such tachycardias manifest with normal QRS complexes, a ventricular rate of more than 200 beats per minute, regular R-R intervals, and a retrograde P wave well beyond the end of QRS.
      • They should be treated in the same way as AVNRT, by blocking AV node conduction with (1) vagal maneuvers (eg, Valsalva maneuver, carotid sinus massage, splashing cold water or ice water on the face), (2) intravenous adenosine, or (3) intravenous verapamil or diltiazem (ie, if recurrent SVT is present, if adenosine is ineffective, or if the patient is taking theophylline).
      • Note that atrial fibrillation can occur after drug administration, particularly adenosine, with a rapid ventricular response. An external cardioverter-defibrillator should be immediately available in case it is necessary.
    • Atrial flutter/fibrillation or wide-complex tachycardia
      • Atrial flutter/fibrillation can be recognized by the presence of abnormal QRS complexes and irregular R-R intervals. In this setting, drugs that prolong the refractory period of the bypass tract should be used, especially those that also block the AV node (by prolonging refractoriness). Examples of such drugs include procainamide (class IA agent) and propranolol (class II beta-blocker).
      • If wide-complex tachycardia is present and the diagnosis of ventricular tachycardia cannot be excluded, the drugs of choice are intravenous procainamide or amiodarone (in lieu of cardioversion if the patient is stable hemodynamically). Ibutilide may also be useful in this setting, although data are lacking.
      • Importantly, avoid lidocaine in this setting. It does not prolong refractoriness in the accessory pathway. Lidocaine may increase the ventricular response if atrial fibrillation is present.
    • Hemodynamically unstable tachycardia and electrical cardioversion
      • In patients with a very fast ventricular rate, hemodynamic instability (eg, hypotension, mental status change) may ensue.
      • The initial treatment of choice in such patients is direct-current synchronized electrical cardioversion.
      • Electrical cardioversion appears to terminate most effectively the tachycardias due to reentry, such as AVNRT and reciprocating tachycardias associated with WPW syndrome.
      • The electrical shock depolarizes all excitable myocardium, lengthens refractoriness, interrupts reentrant circuits, discharges foci, and establishes electrical homogeneity that terminates reentry.
      • Because myocardial damage may occur with increases in applied energy, the minimum effective energy should be used and the energy should be titrated. An energy of at least 100 joules (monophasic or lower biphasic) successfully terminates most SVTs and should be tried initially. If that fails, a second shock with higher energy can be delivered.
      • Cardioversion can have several adverse effects. It may induce arrhythmias because of inadequate synchronization, with the shock occurring during the ST segment or T wave. Rarely, even a properly synchronized shock can produce ventricular fibrillation. Postcardioversion arrhythmias are generally transient and do not require treatment. Embolic episodes may occur in 1-3% of the patients converted from atrial fibrillation to sinus rhythm if the episodes are longer than 48 hours.
  • Long-term maintenance treatment
    • Response to long-term antiarrhythmic therapy for the prevention of further episodes of tachycardia in patients with WPW syndrome remains quite variable and unpredictable. Some drugs may paradoxically make the reciprocating tachycardia more frequent. Dual-drug therapy has been used, eg, procainamide and verapamil (class IA and IV), or quinidine and propranolol (class IA and II). Good reasons exist to avoid quinidine and procainamide; newer drugs that are safer and better are available. Class IC drugs (eg, flecainide, propafenone, moricizine), amiodarone, or sotalol are good choices, but class IC drugs should not be given if the patient has structural heart disease. Class IC drugs are typically used with an AV nodal blocking agent.
    • The best plan is to not use drugs at all; instead, refer all patients who have symptomatic WPW syndrome for ablation because this cures the tachycardia and eliminates the potential dangerous effects of drugs.
    • Patients who have accessory pathways with short refractory periods are poor candidates for medical therapy and are best treated with ablation.

Surgical Care

Ablative procedures are the therapy of choice. Electrode catheters can be advanced intravenously to locate and ablate the accessory tract by delivering electrical or RF energy. Cryothermy, lasers, direct current, and microwave energy sources have also been used in the past, but RF catheter ablation has replaced these modalities because it is much more efficacious, safe, and cost-effective.5

  • RF ablation is currently the treatment of choice for most adults and many children with symptomatic WPW syndrome (ie, those who have AV reentrant tachycardia or atrial flutter/fibrillation with conduction of the accessory pathway). Success rates for catheter ablation exceed 90%.
    • Localization of the bypass tract(s)
      • First, perform an EP study to (1) determine that the bypass tract is part of the tachycardia reentrant circuit, and (2) locate the optimal site for ablation. Pathways can be located in the left or right free wall or septum of the heart. Multiple pathways may be present in approximately 5% of patients.
      • Pathways at all the sites in the heart and in persons of all age groups can be ablated successfully. The RF ablation creates conduction block that can be seen on intracardiac electrogram findings (ie, during the EP study) between the atrial activation and the bypass tract potential.
  • Identification of the ablation site during EP studies
    • During the EP studies, direct recordings of the accessory pathway indicate the optimal site for ablation.
    • The ventricular insertion site is indicated by the earliest onset of the ventricular electrogram in relation to the delta wave.
    • The atrial insertion site is indicated by the region of the shortest VA interval during orthodromic tachycardia (ie, AV reentrant tachycardia) or ventricular pacing.
    • Successful ablation sites show stable fluoroscopic and electrical features. During orthodromic AV reentrant tachycardia, the time between the ventricular and atrial potentials is short and a pathway potential may be observed.
    • Generally, a thermistor-tipped catheter is used, which shows a stable rise in catheter tip temperature, suggesting catheter stability and optimal catheter-tissue contact. Tip temperatures of at least 55 º C are required for permanent elimination of conduction.
  • Indications for RF ablation
    • Patients with symptomatic AV reentrant tachycardia should receive RF ablation.
    • Atrial fibrillation or other atrial tachyarrhythmias that have rapid ventricular response via a bypass tract is an indication for RF ablation procedures.
    • Patients with AV reentrant tachycardia or atrial fibrillation with rapid ventricular rates found incidentally during EP studies for unrelated arrhythmia should undergo RF ablation.
    • Asymptomatic patients with ventricular preexcitation whose livelihood, profession, insurability, or mental well-being may be influenced by unpredictable tachyarrhythmias or in whom such tachyarrhythmias would endanger the public safety should have an RF ablation procedure.
    • Patients with atrial fibrillation and a controlled ventricular response via the bypass tract are candidates for RF ablation.
    • Patients with a family history of sudden cardiac death should undergo RF ablation.
  • Effectiveness of RF ablation: A survey by the North American Society for Pacing and Electrophysiology (NASPE) indicates that ablation is successful. Results are as follows:
    • For left free wall accessory pathways, 2312 of 2527 patients (91%) were cured.
    • For septal accessory pathways, 1115 of 1279 patients (87%) were cured.
    • For right free wall accessory pathways, 585 of 715 patients (82%) were cured.
  • Complications of RF ablation
    • In the United States, complications have been reported in 94 of 4521 patients (2.1%). Of the 4521 patients, 13 died (0.2%).
    • In Europe, the complication rate is reported to be 4.4%. Of 2222 patients, 3 died.
  • Surgical ablation
    • Surgical open heart procedures were more common before RF ablation was developed.
    • Now, RF catheter ablation has virtually eliminated surgical open heart treatments in the vast majority of patients, with the following exceptions:
      • Patients in whom RF catheter ablation (with repeated attempts) fails
      • Patients undergoing concomitant cardiac surgery (possible exception)
      • Patients with other tachycardias with multiple foci who require surgical intervention (very rare)

Consultations

Specific subspecialty consultations are often needed. These may include any of the following:

  • Cardiovascular specialist
  • Electrophysiologist
  • Pediatric cardiovascular specialist

Diet

  • The majority of patients presenting with WPW syndrome are not elderly.
  • Patients presenting with structural heart disease, cardiomyopathy, or heart failure may require a low-salt, low-cholesterol diet.

Activity

Generally, no activity restrictions are recommended in patients with ECG findings of preexcitation but without tachycardias. They should be restricted from high-risk professions (eg, airline pilot) and may be restricted from competitive sports.

  • Patients presenting with tachycardias and accessory pathways should avoid participating in competitive sports because catecholamines can decrease the refractoriness of the bypass tract and facilitate tachyarrhythmias.
  • Patients with hypertrophic cardiomyopathy or the Ebstein anomaly should also abstain from competitive sports.
  • Once a curative procedure (eg, RF ablation of the accessory pathway) has been successfully performed, most patients can return to competitive sports several months later.

Medication

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Antiarrhythmic agents

Prolong refractory period of the conduction tissue, the accessory pathway, or both.


Adenosine (Adenocard)

Blocks conduction time in the AV node. Can interrupt AVRT by blocking conduction in the AV node to restore normal sinus rhythm in PSVT, including PSVT associated with WPW syndrome. Should not be given to patients with preexcitation.

Adult

6 mg rapid IV bolus over 1-2 s initially; if no response within 1-2 min, give 12 mg rapid IV bolus; repeat 12-mg dose second time prn; not to exceed doses >12 mg

Pediatric

0.1 mg/kg IV; repeat at 0.2 mg/kg if first dose not effective; not to exceed 12 mg
Alternatively, 0.05 mg/kg IV; if not effective within 2 min, increase dose by 0.05-mg/kg increments q2min; not to exceed 0.25 mg/kg

Coadministration with carbamazepine may produce higher degrees of heart block; dipyridamole may potentiate effects; methylxanthines may antagonize effects; do not administer to patients with a heart transplant

Documented hypersensitivity; second- or third-degree AV block or sick sinus syndrome (except in patients with functioning artificial pacemaker); atrial flutter; atrial fibrillation; ventricular tachycardia

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Adenosine-induced bronchoconstriction possible in patients with asthma
May cause prolonged asystole in patients with a heart transplant; may provoke atrial fibrillation


Propranolol (Inderal)

Class II antiarrhythmic nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.

Adult

1-3 mg IV under careful monitoring; not to exceed 1 mg/min to avoid lowering blood pressure and causing cardiac standstill; allow time for drug to reach site of action (particularly if slow circulation); administer second dose after 2 min prn thereafter, not to be administered sooner than 4 h after initial dose; do not continue doses after desired alteration in rate or rhythm achieved; switch to PO as soon as clinically indicated; 10-30 mg tid/qid (usual)

Pediatric

2-4 mg/kg/d PO divided bid (ie, 1-2 mg/kg bid); IV use not recommended; however, for arrhythmias, dose of 0.01-0.1 mg/kg by slow push has been recommended; not to exceed 1 mg/dose; change to PO as soon as clinically indicated

Coadministration with aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease effects; calcium channel blockers, cimetidine, loop diuretics, and MAOIs may increase toxicity; toxicity of hydralazine, haloperidol, benzodiazepines, and phenothiazines may increase

Documented hypersensitivity; uncompensated CHF; bradycardia; cardiogenic shock; AV conduction abnormalities

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Beta-adrenergic blockade may decrease signs of acute hypoglycemia and hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor closely


Verapamil (Verelan, Calan)

By interrupting reentry at AV node, can restore normal sinus rhythm in patients with PSVT.

Adult

80-160 mg PO tid; alternatively, 5-10 mg IV followed by second dose 15-30 min later if patient does not respond satisfactorily to initial dose; extended-release dosage form may be given qd

Pediatric

Not established

May increase carbamazepine, digoxin, and cyclosporine levels; coadministration with amiodarone can cause bradycardia and a decrease in cardiac output; when administered concurrently with beta-blockers, may increase cardiac depression; cimetidine may increase levels; may increase theophylline levels

Documented hypersensitivity; severe CHF; sick sinus syndrome or second- or third-degree AV block; hypotension (<90 mm Hg systolic)

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Hepatocellular injury may occur; transient elevations of transaminases with and without concomitant elevations in alkaline phosphatase and bilirubin have occurred (elevations have been transient and may disappear with continued treatment); monitor liver function periodically


Digoxin (Lanoxin)

Has direct inotropic effects in addition to indirect effects on the cardiovascular system. However, may shorten refractory period. Most deaths in WPW have been associated with digoxin use.

Adult

NOT RECOMMENDED; has been associated with ventricular fibrillation

Pediatric

5-10 years: 20-35 mcg/kg PO
>10 years: 10-15 mcg/kg PO
Maintenance dose: 25-35% of PO loading dose

IV calcium may produce arrhythmias in digitalized patients; medications that may increase levels include alprazolam, benzodiazepines, bepridil, captopril, cyclosporine, propafenone, propantheline, quinidine, diltiazem, aminoglycosides, oral amiodarone, anticholinergics, diphenoxylate, erythromycin, felodipine, flecainide, hydroxychloroquine, itraconazole, nifedipine, omeprazole, quinine, ibuprofen, indomethacin, esmolol, tetracycline, tolbutamide, and verapamil
Medications that may decrease serum levels include aminoglutethimide, antihistamines, cholestyramine, neomycin, penicillamine, aminoglycosides, oral colestipol, hydantoins, hypoglycemic agents, antineoplastic treatment combinations (including carmustine, bleomycin, methotrexate, cytarabine, doxorubicin, cyclophosphamide, vincristine, procarbazine), aluminum or magnesium antacids, rifampin, sucralfate, sulfasalazine, barbiturates, kaolin/pectin, and aminosalicylic acid

Documented hypersensitivity; ADULT PATIENTS; beriberi heart disease, idiopathic hypertrophic subaortic stenosis, constrictive pericarditis, and carotid sinus syndrome

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Hypokalemia may reduce positive inotropic effect of digitalis; hypercalcemia predisposes patient to digitalis toxicity, and hypocalcemia can make digoxin ineffective until serum calcium levels are normal; magnesium replacement therapy must be instituted in patients with hypomagnesemia to prevent digitalis toxicity; patients diagnosed with incomplete AV block may progress to complete block when treated with digoxin; exercise caution in hypothyroidism, hypoxia, and acute myocarditis; adjust dose in renal impairment; highly toxic (overdoses can be fatal)


Procainamide (Procanbid, Pronestyl)

Class IA antiarrhythmic. Increases refractory period of atria, ventricles, and accessory pathway. Excellent in preexcited atrial fibrillation or flutter.

Adult

30 mg/min IV continuous infusion until arrhythmia suppressed, patient becomes hypotensive, QRS widens 50% above baseline, or maximum dose of 17 mg/kg administered; once arrhythmia suppressed, may infuse at continuous rate of 1-4 mg/min

Pediatric

Not established; suggested as follows:
15-50 mg/kg/d PO divided q3-6h; not to exceed 4 g/d
20-30 mg/kg/d IM divided q4-6h; not to exceed 4 g/d
3-6 mg/kg/dose IV infused over 5 min
Maintenance dose: 20-80 mcg/kg/min administered as continuous infusion; not to exceed 100 mg/dose or 2 g/d

Can expect increased levels of procainamide metabolite NAPA in patients taking cimetidine, ranitidine, beta-blockers, amiodarone, trimethoprim, and quinidine; may increase effect of skeletal muscle relaxants, quinidine and lidocaine, and neuromuscular blockers; ofloxacin inhibits tubular secretion of procainamide and may increase bioavailability; when taken concurrently with sparfloxacin, may increase risk of cardiotoxicity

Documented hypersensitivity; torsade de pointes; systemic lupus erythematosus

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Monitor for hypotension; plasma concentrations and active metabolite (NAPA) may increase in renal failure; high or toxic concentrations may induce AV block or abnormal automaticity; toxicity may outweigh benefit long term; do not use as a first-line drug for WPW syndrome


Quinidine (Quinaglute, Quinidex, Cardioquin)

Maintains normal heart rhythm and converts atrial fibrillation or flutter. Not recommended as first-line drug for WPW syndrome.

Adult

200 mg PO q2-3h for 5-8 doses with subsequent daily increases until sinus rhythm restored or adverse effects occur; not to exceed 3-4 g/d

Pediatric

30 mg/kg/d PO in 5 divided doses

Phenytoin, rifampin, and phenobarbital may decrease concentrations; toxicity increased when taken with ritonavir, sparfloxacin, beta-blockers, amiodarone, verapamil, cimetidine, alkalinizing agents, or nondepolarizing or depolarizing muscle relaxants; may enhance effect of anticoagulants

Documented hypersensitivity; complete AV block or intraventricular conduction defects; presently taking ritonavir or sparfloxacin

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in G-6-PD deficiency and those with tendency to develop granulocytopenia; avoid use in myocardial depression, hepatic or renal insufficiency, and myasthenia gravis


Amiodarone (Cordarone, Pacerone)

May inhibit AV conduction and sinus node function. Prolongs action potential and refractory period in myocardium and inhibits adrenergic stimulation.

Adult

Loading dose: 800-1600 mg/d PO in 1-2 doses for 1-3 wk; decrease to 600-800 mg/d in 1-2 doses for 1 mo
Maintenance dose: 400 mg/d PO; alternatively, 150 mg (10 mL) IV over first 10 min, followed by 360 mg (200 mL) over next 6 h, then 540 mg over next 18 h

Pediatric

10-15 mg/kg/d or 600-800 mg/1.73 m2/d PO for 4-14 d or until adequate control of arrhythmia attained

Increases effect and blood levels of theophylline, quinidine, procainamide, phenytoin, methotrexate, flecainide, digoxin, cyclosporine, beta-blockers, and anticoagulants; cardiotoxicity increased by ritonavir, sparfloxacin, and disopyramide; coadministration with calcium channel blockers may cause additive effect and further decrease myocardial contractility; cimetidine may increase level

Documented hypersensitivity; complete AV block; intraventricular conduction defects; taking ritonavir or sparfloxacin

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in thyroid or liver disease


Sotalol (Betapace)

Class III antiarrhythmic agent that blocks potassium channels, prolongs action potential duration, and lengthens QT interval. Noncardiac selective beta-adrenergic blocker.

Adult

80 mg PO bid; increase dose gradually q2-3d to 240-320 mg/d

Pediatric

Not established

Aluminum salts, barbiturates, NSAIDs, penicillins, calcium salts, cholestyramine, and rifampin may decrease bioavailability and plasma levels, possibly resulting in decreased pharmacologic effect; cardiotoxicity may increase when administered concurrently with sparfloxacin, calcium channel blockers, quinidine, flecainide, and contraceptives; toxicity increases when administered concurrently with digoxin, flecainide, acetaminophen, clonidine, epinephrine, nifedipine, prazosin, haloperidol, phenothiazines, and catecholamine-depleting agents

Documented hypersensitivity; long QT, history of torsades de pointes

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

Beta-adrenergic blockade may decrease signs and symptoms of acute hypoglycemia and clinical signs of hyperthyroidism; abrupt withdrawal may exacerbate symptoms of hyperthyroidism, including thyroid storm; withdraw drug slowly and monitor patient closely; caution in hypokalemia, peripheral vascular disease, hypomagnesemia, and CHF


Diltiazem (Cardizem, Dilacor, Tiamate, Tiazac)

Slows AV nodal conduction.

Adult

IR: 30-90 mg PO q8h
SR: 120-300 mg PO qd
IV: 10-20 mg bolus over 10-20 min, followed by continuous infusion at 10-15 mg/h

Pediatric

Not established

May increase carbamazepine, digoxin, cyclosporine, and theophylline levels; when administered with amiodarone, may cause bradycardia and decrease in cardiac output; when given with beta-blockers, may increase cardiac depression; cimetidine may increase levels

Documented hypersensitivity; severe CHF; sick sinus syndrome; second- or third-degree AV block; hypotension (<90 mm Hg systolic)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in impaired renal or hepatic function; may increase LFT levels, and hepatic injury may occur


Ibutilide (Corvert)

Class III antiarrhythmic agent that may work by increasing action potential duration, thereby changing atrial cycle length variability. Mean time to conversion is 30 min. Two thirds of patients who converted were in sinus rhythm at 24 h. Ventricular arrhythmias occurred in 9.6% of patients and were mostly PVCs. The incidence of torsades de pointes was <2%.

Adult

<60 kg: 0.01 mg/kg IV over 10 min
>60 kg: 1 mg IV over 10 min

Pediatric

Not established

Increases toxicity of quinidine and procainamide; concurrent administration with TCAs and phenothiazines may prolong QT interval; toxicity of digoxin increases when administered concurrently

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in renal or hepatic impairment


Dofetilide (Tikosyn)

Increases monophasic action potential duration, primarily due to delayed repolarization. Terminates induced reentrant tachyarrhythmias (eg, atrial fibrillation/flutter, ventricular tachycardia) and prevents their reinduction. No data in WPW syndrome.

Adult

125-500 mcg IV bid; must be started in an inpatient monitored setting

Pediatric

Not established

Verapamil, TMP/SMZ, ketoconazole, potassium-depleting diuretics, digoxin, cimetidine, phenothiazines, triamterene, metformin, prochlorperazine, amiloride, megestrol, and antiarrhythmic agents may increase toxicity

Documented hypersensitivity; concomitant use of verapamil or the cation transport system inhibitor cimetidine, trimethoprim (alone or in combination with sulfamethoxazole), or ketoconazole; congenital or acquired long QT syndromes; severe renal impairment (CrCl <20 mL/min); prochlorperazine and megestrol coadministration; a baseline QT interval or QTc >440 ms (500 ms in patients with ventricular conduction abnormalities)

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Maintain potassium levels within reference range prior to and during administration; to minimize risk of induced arrhythmia, calculations of CrCl and continuous ECG monitoring required; cardiac resuscitation equipment and personnel must be present


Flecainide (Tambocor)

Blocks sodium channels, producing dose-related decrease in intracardiac conduction in all parts of heart. Increases electrical stimulation of threshold of ventricle, His-Purkinje system. Shortens phase 2 and phase 3 repolarization, resulting in decreased action potential duration and ERP.
Indicated for the treatment of paroxysmal atrial fibrillation/flutter associated with disabling symptoms and PSVT, including AVNRT, AV reentrant tachycardia, and other SVTs of unspecified mechanism associated with disabling symptoms in patients without structural heart disease. Also indicated for prevention of documented life-threatening ventricular arrhythmias, such as sustained ventricular tachycardia.
Not recommended in less severe ventricular arrhythmias, even if patients are symptomatic.

Adult

100 mg PO bid q12h; increase q4d but not to exceed 400 mg/d

Pediatric

3-6 mg/kg/d or 100-150 mg/m2/d divided tid to 11 mg/kg/d or 200 mg/m2/d

May increase toxicity of digoxin; beta-adrenergic blockers, verapamil, and disopyramide may have additive inotropic effects when administered with flecainide; CYP4502D6 inhibitors (eg, ritonavir, cimetidine, amiodarone) may increase serum levels and cardiotoxicity

Documented hypersensitivity; preexisting second- or third-degree AV block, RBBB associated with left hemiblock (bifascicular block) or trifascicular block, unless a pacemaker is present to sustain cardiac rhythm if complete heart block occurs; concurrent use of ritonavir or amprenavir; recent MI

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in preexisting sinus node dysfunction, history of CHF, sick sinus syndrome, post MI, or myocardial dysfunction; reserve use for life-threatening arrhythmias only because deaths have been associated with proarrhythmic effects of class IC antiarrhythmics; typically used in conjunction with an AV nodal blocking agent; adjust dose in renal or hepatic impairment


Propafenone (Rythmol)

Shortens upstroke velocity (phase 0) of monophasic action potential. Reduces fast inward current carried by sodium ions in Purkinje fibers and, to a lesser extent, myocardial fibers. May increase diastolic excitability threshold and prolong ERP. Reduces spontaneous automaticity and depresses triggered activity. Indicated for treatment of documented life-threatening ventricular arrhythmias, such as sustained ventricular tachycardia. Appears to be effective in the treatment of SVTs, including atrial fibrillation and flutter. Not recommended in patients with less severe ventricular arrhythmias, even if patients are symptomatic.

Adult

150 mg PO q8h; increase at 3- to 4-d intervals, not to exceed 300 mg q8h

Pediatric

Not established

Rifampin may decrease plasma levels; quinidine may increase pharmacologic effects; may increase plasma levels of beta-blockers, cyclosporine, warfarin, and digoxin; CYP4502D6 inhibitors (eg, ritonavir, cimetidine, amiodarone) may increase serum levels and cardiotoxicity

Documented hypersensitivity, second- or third-degree AV block, right bundle-branch block associated with left hemi-block (bifascicular block) or trifascicular block; concurrent use of ritonavir or amprenavir

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Caution in preexisting sinus node dysfunction, history of CHF, sick sinus syndrome, post MI, or myocardial dysfunction; reserve use for life-threatening arrhythmias only because deaths have been associated with proarrhythmic effects of class IC antiarrhythmics; adjust dose in renal or hepatic impairment; typically used in conjunction with an AV nodal blocking agent

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References
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References

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  2. Sethi KK, Dhall A, Chadha DS, Garg S, Malani SK, Mathew OP. WPW and preexcitation syndromes. J Assoc Physicians India. Apr 2007;55 Suppl:10-5. [Medline].

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Further Reading

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Keywords

Wolff-Parkinson-White syndrome, preexcitation syndrome, pre-excitation syndrome, atrio-ventricular re-entrant tachycardia, atrioventricular reentrant tachycardia, AVRT, AVNRT, atrioventricular nodal reentrant tachycardia, AV nodal reentrant tachycardia, WPW syndrome, paroxysmal supraventricular tachycardia, PSVT, supraventricular tachycardia, SVT, heart disease

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Contributor Information and Disclosures

Author

Vibhuti N Singh, MD, MPH, FACC, FSCAI, Director, Suncoast Cardiovascular Center; Chair, Cardiology Division and Cath Labs, Department of Medicine, Bayfront Medical Center; Clinical Assistant Professor, Division of Cardiology, University of South Florida College of Medicine
Vibhuti N Singh, MD, MPH, FACC, FSCAI is a member of the following medical societies: American College of Cardiology, American College of Physicians, American Heart Association, American Medical Association, and Florida Medical Association
Disclosure: Nothing to disclose.

Coauthor(s)

Rakesh K Sharma, MD, FACC, Adjunct Associate Professor of Medicine and Cardiology; University of Arkansas for Medical Sciences, Medical Center of South Arkansas
Rakesh K Sharma, MD, FACC is a member of the following medical societies: American College of Cardiology, American College of International Physicians, American College of Physicians, American Heart Association, and American Medical Association
Disclosure: Nothing to disclose.

Medical Editor

Russell F Kelly, MD, Program Director, Assistant Professor, Department of Internal Medicine, Division of Cardiology, Cook County Hospital, Rush Medical College
Russell F Kelly, MD is a member of the following medical societies: American College of Cardiology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: eMedicine Salary Employment

Managing Editor

Brian Olshansky, MD, Professor of Medicine, Department of Internal Medicine, University of Iowa College of Medicine
Brian Olshansky, MD is a member of the following medical societies: American Autonomic Society, American College of Cardiology, American College of Chest Physicians, American College of Physicians, American College of Sports Medicine, American Federation for Clinical Research, American Heart Association, Cardiac Electrophysiology Society, Heart Rhythm Society, and New York Academy of Sciences
Disclosure: Guidant/Boston Scientific Honoraria Speaking and teaching; Medtronic Honoraria Speaking and teaching; Guidant/Boston Scientific Consulting fee Consulting; Reliant Grant/research funds Other; Novartis Honoraria Speaking and teaching; Novartis Consulting fee Consulting

CME Editor

Amer Suleman, MD, Consultant in Electrophysiology and Cardiovascular Medicine, Department of Internal Medicine, Division of Cardiology, Medical City Dallas Hospital
Amer Suleman, MD is a member of the following medical societies: American College of Physicians, American Heart Association, American Institute of Stress, American Society of Hypertension, Federation of American Societies for Experimental Biology, Royal Society of Medicine, and Society of Cardiac Angiography and Interventions
Disclosure: Nothing to disclose.

Chief Editor

Jeffrey N Rottman, MD, Professor of Medicine and Pharmacology, Director, Clinical Cardiac Electrophysiology Fellowship Program, Vanderbilt University School of Medicine; Chief, Department of Cardiology, Nashville Veterans Affairs Medical Center
Jeffrey N Rottman, MD is a member of the following medical societies: American Heart Association and North American Society of Pacing and Electrophysiology (NASPE)
Disclosure: Nothing to disclose.

 
 
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