This combination of atrial fibrillation and WPW is considered dangerous, and most antiarrhythmic drugs are contraindicated.When an individual is in normal sinus rhythm, the ECG characteristics of WPW are a short PR interval (less than 120 milliseconds in duration), widened QRS complex (greater than 120 milliseconds in duration) with slurred upstroke of the QRS complex, and secondary repolarization changes (reflected in ST segment-T wave changes).In individuals with WPW, electrical activity that is initiated in the SA node travels through the accessory pathway, as well as through the AV node to activate the ventricles via both pathways. Since the accessory pathway does not have the impulse slowing properties of the AV node, the electrical impulse first activates the ventricles via the accessory pathway, and immediately afterwards via the AV node. This gives the short PR interval and slurred upstroke of the QRS complex known as the delta wave.In case of type A pre-excitation (left atrioventricular connections), a positive R wave is seen in V1 ("positive delta") on the precordial leads of the electrocardiogram, while in type B pre-excitation (right atrioventricular connections), a predominantly negative delta wave is seen in lead V1 ("negative delta").People with WPW may have more than one accessory pathway – in some cases, as many as eight abnormal pathways have been found. This has been seen in individuals with Ebsteins anomaly.Wolff–Parkinson–White syndrome is sometimes associated with Lebers hereditary optic neuropathy, a form of mitochondrial disease. Risk stratification
WPW carries a small risk of sudden death, presumably due to rapidly conducted atrial fibrillation causing ventricular fibrillation.
However, if there is any doubt about the diagnosis of orthodromic AVRT or if aberrant conduction leading to a wide complex QRS is observed, it may be prudent to manage as undifferentiated wide complex tachycardia. People with atrial fibrillation and rapid ventricular response may be treated with amiodarone or procainamide to stabilize their heart rate. Procainamide and cardioversion are accepted treatments for conversion of tachycardia found with WPW. Amiodarone in atrial fibrillation with WPW, is linked to ventricular fibrillation, and thus may be worse than procainamide.AV node blockers should be avoided in atrial fibrillation and atrial flutter with WPW or history of it; this includes adenosine, diltiazem, verapamil, other calcium channel blockers, and beta blockers. They can exacerbate the syndrome by blocking the hearts normal electrical pathway (therefore favoring 1:1 atrial to ventricle conduction through the pre-excitation pathway, potentially leading to unstable ventricular arrhythmias). Catheter ablation
The definitive treatment of WPW is the destruction of the abnormal electrical pathway by catheter ablation. Two main types of catheter ablation include radiofrequency ablation with heat or cryoablation with cold energy. This procedure is performed by cardiac electrophysiologists and has high success rate in the hands of an experienced electrophysiologist. Findings from 1994 indicate success rates of as high as 95% in people treated with radiofrequency catheter ablation for WPW. If radiofrequency catheter ablation is successfully performed, the condition is generally considered cured. Recurrence rates are typically less than 5% after a successful ablation.