The above syndrome is basically due to pre-excitation of the ventricles secondary to an accessory conduction pathway between the atria and ventricles.
By pre-excitation, I mean that the ventricles are depolarised earlier than they would have been, had there only been the normal conduction pathway between the atria and ventricles. Recall the conduction pathway of the heart. An impulse starts at the sino-atrial node in the right atrium, and is propagated throughout both atria. By this manner, it reaches the atrio-ventricular node (AV node), which sits at the junction of the atria and ventricles and acts as a 'gatekeeper' to the ventricles. Under normal circumstances, the only way for an electrical impulse to reach the ventricles is through this node. The node also slows the impulse down, and makes sure that impulses don't pass through to the ventricles too quickly.
In Wolff-Parkinson-White syndrome, however, there exists an additional pathway (sometimes called the bundle of Kent) linking the atria to the ventricles. This pathway has none of the specialised features of the AV node, and happily allows impulses from the atria through to the ventricles without the AV node's customary delay. Thus, on E.C.G., there is a shortened PR interval: pre-excitation.
If the atrial impulses happen to come too quickly, as in atrial flutter or atrial fibrillation, then the ventricles, left unprotected due to the bypassing of the AV node, will automatically contract too quickly as well. Thus, there is a predisposition to tachyarrhythmias.
Patients with WPW syndrome may be asymptomatic, in which case they don't usually require treatment, or symptomatic, in which case they do usually require treatment. Treatment is tricky and depends on whether or not the patient is stable. The only definitive treatment is for the accessory pathway to be ablated.