Atrial Fibrillation and Wolff-Parkinson-White Syndrome (WPW)
In manifest Wolff-Parkinson-White (WPW) syndrome, antegrade conduction occurs over the accessory pathway. If atrial fibrillation develops, the normal rate-limiting effects of the atrioventricular (AV) node are bypassed, and the resultant excessive ventricular rates (sometimes 200 to 240 beats/minutes) 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.
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.