Country cardiograms case 2: Wolff-Parkinson-White syndrome Can J Rural Med 1996; 1 (2): 99-100
The patient had a WPW accessory pathway in his heart between the atria and the ventricles, which bypassed the atrioventricular (AV) node (Fig. 1). The ECG had been normal for several years before this presentation because conduction had been occurring normally down the usual pathways from the sinoatrial node to the AV node, the accessory pathway being electrocardiographically silent.
The abnormal ECG was obtained on a day when the accessory pathway was active. Conduction was occurring from the atria directly into the ventricular tissue, without going through the AV node first. The delta wave occurred because the accessory pathway terminated directly in ventricular tissue, and part of the ventricular tissue depolarized early (pre-excitation), shortening the usual PR interval. Therefore, the ECG did not show the PR interval refractory period normally produced by the AV node. The QRS complex was widened because ventricular depolarization was occurring more slowly than if conduction had occurred rapidly down the normal conduction fibres.
In spite of being rare in the population as a whole, accessory pathways are present in about 30% of cases of paroxysmal supraventricular tachycardia (PSVT).[4] Consequently, WPW is a concern every time a patient presents with tachycardia. Two common agents for treating PSVT, verapamil and digoxin, can accelerate conduction down the accessory pathway into the ventricles, particularly in WPW atrial fibrillation, producing ventricular fibrillation.
Patients with WPW syndrome commonly present to the emergency department with narrow-QRS PSVT, caused by normal downward conduction from the atria to the AV node. The upward re-entry conduction occurs back into the atria through the accessory pathway. Verapamil can terminate, effectively and safely, PSVT in patients with WPW syndrome who have this kind of conduction, although even in these cases there is a theoretical risk of triggering ventricular fibrillation. We have discovered that over the past decade we inadvertently treated with verapamil two patients who had silent WPW accessory pathways, without adverse effects. However, adenosine and procainamide are safer.[4]
Rarely, patients with WPW syndrome may present with wide-complex tachycardia, caused when downward conduction to the ventricles occurs through the accessory pathway. The upward re-entrant conduction occurs back into the atria through the AV node. Verapamil can cause this arrhythmia to degrade into ventricular fibrillation.
About 10% to 30% of arrhythmias in WPW syndrome are atrial fibrillation and therefore are irregularly irregular.[5] Atrial fibrillation in WPW syndrome can occur with narrow, wide or mixed-width QRS complexes. When the tachycardia is very fast, it can be difficult to differentiate atrial fibrillation from supraventricular tachycardia. As explained previously, verapamil and digoxin are contraindicated in atrial fibrillation when a WPW accessory pathway is present. Fortunately, rural physicians will face this problem only rarely, since the great majority of atrial fibrillation is not due to WPW syndrome. However, WPW syndrome is a distinct possibility in cases of atrial fibrillation in younger patients and in patients with wide or mixed-width QRS complexes.
Antiarrhythmic agents such as flecainide, propafenone and amiodarone slow accessory pathway conduction; therefore, they probably have a role in the management of WPW syndrome.[6] As electrophysiologists learn more about them, these newer antiarrhythmic agents are likely to appear in rural hospital formularies and Advanced Cardiac Life Support protocols.
Patients with WPW syndrome can experience supraventricular tachycardia, atrial fibrillation and sudden death.[7] Interestingly, about one in eight people with WPW syndrome eventually loses any ECG evidence of the accessory pathway.[1] For this reason, and because the risk of sudden death is extremely low in asymptomatic patients, asymptomatic young patients are usually not treated.[8]
Radiofrequency ablation of the accessory pathway is now considered the initial nonpharmacologic treatment of choice for symptomatic patients.[6] The procedure is quick, involving little or no anesthesia, and frees the patient from lifelong medication.
This young man's cardiologists decided to give him sotalol, and they will ablate the accessory pathway when he turns 18 years of age. The patient was advised to wear an alert bracelet, so that he could be treated appropriately if he presented with arrhythmia in the meantime.