Wolff-Parkinson-White Syndrome Medication
- Author: Christopher Randall Ellis, MD; Chief Editor: Jeffrey N Rottman, MD more...
Medication Summary
Emergency treatment in Wolff-Parkinson-White (WPW) patients with hemodynamic instability is directed toward converting the rhythm to sinus through a brief episode of atrioventricular (AV) block. Adenosine is the drug of choice for immediate conversion of narrow-complex supraventricular tachycardia (SVT) but should not be used for preexcited atrial fibrillation (AF). Esmolol has also been used with some success.
Beta-blockers are probably the medications most commonly used to treat SVT in the presence of preexcitation. They are moderately effective and have frequent, but rarely life-threatening, adverse effects (except in the presence of reactive airway disease). Their efficacy in reducing the risk of accelerated conduction of AF in WPW patients is unclear. More potent medications (eg, flecainide, propafenone, sotalol, or amiodarone) may have more effect on accessory pathway (AP) conduction or refractoriness than beta-blockers and are preferred by some.
The use of digoxin or verapamil for long-term therapy appears to be contraindicated for many patients with WPW syndrome, because these medications may enhance antegrade conduction through the AP by increasing the refractory period in the AV node. In addition, digoxin may shorten the refractory period of the AP, further enhancing its antegrade conduction.
Antiarrhythmic Agents
Class Summary
Antiarrhythmic agents alter the electrophysiologic mechanisms responsible for dysrhythmia, prolonging the refractory period of the conduction tissue, the AP, or both.
Adenosine (Adenocard, Adenoscan)
Adenosine slows conduction time through the AV node. It can interrupt atrioventricular reentrant tachycardia (AVRT) by blocking conduction in the AV node to restore normal sinus rhythm in paroxysmal supraventricular tachycardia (PSVT), including PSVT associated with WPW syndrome. It should not be given to patients with preexcitation unless by a cardiac electrophysiologist.
Verapamil (Verelan, Calan)
Verapamil interrupts reentry at the AV node and restores normal sinus rhythm in patients with PSVT. It is used for short-term treatment only in children older than 2 years. It is not intended for long-term treatment, because of a shortened refractory period. Do not use it in children younger than 2 years, because of severe hypotension.
Digoxin (Lanoxin)
Digoxin has direct inotropic effects in addition to indirect effects on the cardiovascular system. However, it may shorten the refractory period. Most deaths in WPW have been associated with digoxin use.
Procainamide
Procainamide is a class Ia antiarrhythmic. It increases the refractory period of atria, ventricles, and APs. It is excellent in preexcited AF or atrial flutter.
Quinidine
Quinidine maintains normal heart rhythm and converts AF or atrial flutter. It is not recommended as a first-line drug for WPW syndrome.
Amiodarone (Cordarone, Pacerone)
Amiodarone may inhibit AV conduction and sinus node function. It prolongs the action potential and refractory period in myocardium and inhibits adrenergic stimulation.
Sotalol (Betapace, Sorine)
Sotalol is a class III antiarrhythmic agent that blocks potassium channels, prolongs action potential duration, and lengthens the QT interval. It is a noncardiac selective beta-adrenergic blocker.
Diltiazem (Cardizem, Dilacor, Cartia XT, Tiazac)
Diltiazem slows AV nodal conduction.
Ibutilide (Corvert)
Ibutilide is a class III antiarrhythmic agent that may work by increasing action potential duration, thereby changing atrial cycle length variability. Mean time to conversion is 30 minutes. Two thirds of patients who converted were in sinus rhythm at 24 hours. Ventricular arrhythmias occurred in 9.6% of patients and were mostly premature ventricular complexes (PVCs). The incidence of torsades de pointes was less than 2%.
Dofetilide (Tikosyn)
Dofetilide increases monophasic action potential duration, primarily through delayed repolarization. It terminates induced reentrant tachyarrhythmias (eg, AF, atrial flutter, ventricular tachycardia [VT]) and prevents their reinduction. No data are available on its use in WPW syndrome.
Flecainide (Tambocor)
Flecainide blocks sodium channels, producing dose-related decreases in intracardiac conduction in all parts of heart. It has its greatest effect on the His-Purkinje system (HV conduction). Effects on AV nodal conduction time and intra-atrial conduction times, though present, are less pronounced than those on ventricular conduction velocity.
Flecainide is indicated for the treatment of paroxysmal AF or atrial flutter associated with disabling symptoms and PSVT, including AV nodal reentrant tachycardia (AVNRT), AVRT, and other SVTs of unspecified mechanism associated with disabling symptoms in patients without structural heart disease. It is also indicated for prevention of documented life-threatening ventricular arrhythmias, such as sustained VT. It is not recommended in less severe ventricular arrhythmias, even if patients are symptomatic.
Propafenone (Rythmol)
Propafenone shortens the upstroke velocity (phase 0) of a monophasic action potential. It reduces the fast inward current carried by sodium ions in Purkinje fibers and, to a lesser extent, myocardial fibers. It may increase the diastolic excitability threshold and prolong the effective refractory period (ERP). It reduces spontaneous automaticity and depresses triggered activity.
Propafenone is indicated for treatment of documented life-threatening ventricular arrhythmias, such as sustained VT. It appears to be effective in the treatment of SVTs, including AF and atrial flutter. It is not recommended in patients with less severe ventricular arrhythmias, even if they are symptomatic.
Esmolol (Brevibloc)
Esmolol is an ultra–short-acting agent that selectively blocks beta1-receptors, with little or no effect on beta2-receptor types. It is excellent for patients at risk of complications from beta-blockade, particularly those with reactive airway disease, mild-to-moderate left ventricular dysfunction, and/or peripheral vascular disease. Its short half-life of 8 minutes allows for titration to desired effect and quick discontinuation if needed.
Propranolol (Inderal LA, InnoPran XL)
Propranolol is a class II antiarrhythmic nonselective beta-adrenergic receptor blocker with membrane-stabilizing activity that decreases automaticity of contractions.
Atenolol (Tenormin)
Atenolol selectively blocks beta1-receptors with little or no effect on beta2 types.
Wolff, L., Parkinson, J., White, PD. Bundle-branch block with short P-R interval in healthy young people prone to paroxysmal tachycardia. American Heart Journal. 1930/08;5:685-704.
Durrer D, Schuilenburg RM, Wellens HJ. Pre-excitation revisited. Am J Cardiol. Jun 1970;25(6):690-7. [Medline].
Calkins H, Sousa J, el-Atassi R, et al. Diagnosis and cure of the Wolff-Parkinson-White syndrome or paroxysmal supraventricular tachycardias during a single electrophysiologic test. N Engl J Med. Jun 6 1991;324(23):1612-8. [Medline].
Pappone C, Vicedomini G, Manguso F, et al. Risk of malignant arrhythmias in initially symptomatic patients with wolff-Parkinson-white syndrome: results of a prospective long-term electrophysiological follow-up study. Circulation. Feb 7 2012;125(5):661-8. [Medline].
Pappone C, Santinelli V, Manguso F, Augello G, Santinelli O, Vicedomini G. A randomized study of prophylactic catheter ablation in asymptomatic patients with the Wolff-Parkinson-White syndrome. N Engl J Med. Nov 6 2003;349(19):1803-11. [Medline].
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].
Ehtisham J, Watkins H. Is Wolff-Parkinson-White syndrome a genetic disease?. J Cardiovasc Electrophysiol. Nov 2005;16(11):1258-62. [Medline].
Gollob MH, Green MS, Tang AS, Gollob T, Karibe A, Ali Hassan AS. Identification of a gene responsible for familial Wolff-Parkinson-White syndrome. N Engl J Med. Jun 14 2001;344(24):1823-31. [Medline].
Brembilla-Perrot B, Yangni N'da O, Huttin O, Chometon F, Groben L, Christophe C. Wolff-Parkinson-White syndrome in the elderly: clinical and electrophysiological findings. Arch Cardiovasc Dis. Jan 2008;101(1):18-22. [Medline].
Zhang Y, Wang L. Atrial vulnerability is a major mechanism of paroxysmal atrial fibrillation in patients with Wolff-Parkinson-White syndrome. Med Hypotheses. 2006;67(6):1345-7. [Medline].
Szumowski L, Walczak F, Urbanek P, Szufladowicz E, Ratajska E, Kepski R, et al. Risk factors of atrial fibrillation in patients with Wolff-Parkinson-White syndrome. Kardiol Pol. Mar 2004;60(3):206-16; discussion 217. [Medline].
Bromberg BI, Lindsay BD, Cain ME, Cox JL. Impact of clinical history and electrophysiologic characterization of accessory pathways on management strategies to reduce sudden death among children with Wolff-Parkinson-White syndrome. J Am Coll Cardiol. Mar 1 1996;27(3):690-5. [Medline].
Attoyan C, Haissaguerre M, Dartigues JF, Le Métayer P, Warin JF, Clémenty J. [Ventricular fibrillation in Wolff-Parkinson-White syndrome. Predictive factors]. Arch Mal Coeur Vaiss. Jul 1994;87(7):889-97. [Medline].
Mark DG, Brady WJ, Pines JM. Preexcitation syndromes: diagnostic consideration in the ED. Am J Emerg Med. Sep 2009;27(7):878-88. [Medline].
Fengler BT, Brady WJ, Plautz CU. Atrial fibrillation in the Wolff-Parkinson-White syndrome: ECG recognition and treatment in the ED. Am J Emerg Med. Jun 2007;25(5):576-83. [Medline].
Arruda, Mauricio S., et al. Development and validation of an ECG algorithm for identifying accessory pathway ablation site in Wolff-Parkinson-White syndrome. Journal of Cardiovascular Electrophysiology. 1998/01;9:2-12.
Burnes JE, Taccardi B, Rudy Y. A noninvasive imaging modality for cardiac arrhythmias. Circulation. Oct 24 2000;102(17):2152-8. [Medline]. [Full Text].
Ghosh S, Avari JN, Rhee EK, Woodard PK, Rudy Y. Hypertrophic cardiomyopathy with preexcitation: insights from noninvasive electrocardiographic imaging (ECGI) and catheter mapping. J Cardiovasc Electrophysiol. Nov 2008;19(11):1215-7. [Medline]. [Full Text].
Pappone C, Manguso F, Santinelli R, Vicedomini G, Sala S, Paglino G. Radiofrequency ablation in children with asymptomatic Wolff-Parkinson-White syndrome. N Engl J Med. Sep 16 2004;351(12):1197-205. [Medline].
Sarubbi B, D'Alto M, Vergara P, Calvanese R, Mercurio B, Russo MG, et al. Electrophysiological evaluation of asymptomatic ventricular pre-excitation in children and adolescents. Int J Cardiol. Feb 15 2005;98(2):207-14. [Medline].
Duszanska A, Lenarczyk R, Kowalski O, Streb W, Kukulski T, Kalarus Z. Evaluation of left ventricular systolic and diastolic function in patients with atrioventricular re-entrant tachycardia treated by radiofrequency current ablation. Acta Cardiol. Apr 2008;63(2):221-7. [Medline].
Jackman WM, Wang XZ, Friday KJ, et al. Catheter ablation of accessory atrioventricular pathways (Wolff- Parkinson-White syndrome) by radiofrequency current. N Engl J Med. Jun 6 1991;324(23):1605-11. [Medline].
Pappone C, Radinovic A, Santinelli V. Sudden death and ventricular preexcitation: is it necessary to treat the asymptomatic patients?. Curr Pharm Des. 2008;14(8):762-5. [Medline].
Print
