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Atrial Fibrillation and Wolff-Parkinson-White Syndrome (WPW)

By L. Brent Mitchell, MD, Professor of Medicine, Department of Cardiac Services, Libin Cardiovascular Institute of Alberta, University of Calgary

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Patient Education

Atrial fibrillation is a medical emergency when rapid antegrade conduction over an accessory pathway occurs in Wolff-Parkinson-White syndrome.

In manifest Wolff-Parkinson-White (WPW) syndrome, antegrade conduction occurs over the accessory pathway. If atrial fibrillation (AF) develops, the normal rate-limiting effects of the atrioventricular (AV) node are bypassed, and the resultant excessive ventricular rates (sometimes 200 to 240 beats/min) may lead to ventricular fibrillation (see Figure: Atrial fibrillation in Wolff-Parkinson-White syndrome.) and sudden death. Patients with concealed WPW syndrome are not at risk because in them, antegrade conduction does not occur over the accessory connection.

Atrial fibrillation in Wolff-Parkinson-White syndrome.

Ventricular response is very fast (RR intervals minimum of 160 msec). Shortly thereafter, ventricular fibrillation develops (lead II continuous rhythm strip at bottom).


  • Direct-current cardioversion

The treatment of choice for Wolff-Parkinson-White syndrome is direct-current cardioversion. The usual rate-slowing drugs used in atrial fibrillation are not effective, and digoxin and the nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem) are contraindicated because they may increase the ventricular rate and cause ventricular fibrillation. If cardioversion is impossible, drugs that prolong the refractory period of the accessory connection should be used. IV procainamide or amiodarone is preferred, but any class Ia, class Ic, or class III antiarrhythmic drug can be used.

Pearls & Pitfalls

  • Do not give digoxin or nondihydropyridine calcium channel blockers (eg, verapamil, diltiazem) to patients with atrial fibrillation and WPW because these drugs may trigger ventricular fibrillation.

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