Wolff–Parkinson–White Syndrome



The Wolff–Parkinson–White (WPW) syndrome is caused by an accessory ­atrioventricular (AV) pathway that bypasses the AV node, thereby pre-exciting ventricular myocardium. It is characterised by a short PR interval and a delta wave. AV re-entrant tachycardia and atrial fibrillation can result.
    During AV re-entrant tachycardia there will be no delta waves, unless in its rare antidromic form, and treatment is the same whether or not there is pre-excitation. result.
    During atrial fibrillation, the ventricular rate is often very fast, most complexes will usually have a delta wave configuration and there is a risk of ventricular fibrillation when the minimum interval between delta waves is less than 250 ms. Digoxin and verapamil may be dangerous: a drug which slows conduction in the accessory pathway should be used, e.g. sotalol or flecainide. result.
    Radiofrequency catheter ablation should be considered in all symptomatic patients, and in some circumstances in patients with asymptomatic pre-excitation.





Pre-excitation


Wolff–Parkinson–White (WPW) syndrome is due to an accessory AV pathway: the same pathway that, as discussed in Chapter 9, is the cause of AV re-entrant tachycardia (AVRT). The connection, also referred to as a bundle of Kent, is a strand of normal myocardium that traverses the groove between atria and ventricles. It is congenital in origin.


To facilitate AV re-entrant tachycardia it is only necessary for the accessory pathway to conduct in a retrograde direction, i.e. from ventricles to atria. Many patients with AV re-entrant tachycardia have an accessory AV pathway that is only capable of ventriculoatrial conduction. In patients with WPW syndrome the pathway is also capable of anterograde conduction, i.e. from atria to ventricles. Unlike the AV node, the accessory connection does not delay conduction between atria and ventricles: consequently the PR interval is very short, and hence the term pre-excitation.


Normally the atria become electrically isolated from the ventricles during fetal development, apart from the AV junction, i.e. AV node plus bundle of His. Incomplete separation leads to an accessory AV pathway. Rarely, WPW syndrome is familial.


The accessory pathway may be situated anywhere across the groove between atria and ventricles. The most common site is the left free wall of the heart. Other locations are posteroseptal, right free wall and rarely anteroseptal. In a minority of patients there is more than one accessory pathway.


Approximately 1.3–3 per 1000 of the population have the electrocardiographic signs of pre-excitation, two-thirds of whom will experience cardiac arrhythmias. One survey reported 4 per 100 000 newly diagnosed cases per annum. The syndrome is more common in young people. With age, fibrosis may sometimes develop in the AV groove and block an accessory pathway.


ECG characteristics


The characteristics of WPW syndrome are a short PR interval, a widened QRS ­complex due to the presence of a delta wave, and paroxysmal tachycardia (Figure 10.1). If tachycardia has not occurred, then, strictly speaking, the patient has ventricular pre-excitation but not WPW syndrome.


During sinus rhythm, an atrial impulse will reach the ventricles via both the accessory pathway and the normal AV node. The AV node conducts relatively slowly. Therefore initial ventricular activation is solely due to accessory pathway conduction, resulting in a short PR interval: ventricular pre-excitation. Because the accessory pathway is not connected to the His–Purkinje system, the rate of early ventricular activation will be slow, leading to slurring of the ventricular complex, i.e. a delta wave, rather than the brisk upstroke that would result from rapid ventricular activation via the specialised conducting tissues. Once the atrial impulse has traversed the AV node, further ventricular activation will proceed rapidly via the His–Purkinje system. During sinus rhythm, therefore, the ventricular complex is a fusion between delta wave and normal QRS complex (Figure 10.1).


Location of the accessory pathway


The syndrome is classified into types A and B, depending on the ventricular complex in lead V1. If predominantly positive, it is type A (Figures 10.2, 10.3), and if negative, type B (Figure 10.4).


Type A is caused by a left-sided accessory pathway. However, type B is not necessarily due to a right-sided pathway, especially if the delta wave is small.


Complex ECG algorithms have been devised for precise location of accessory pathways, but none is reliable. There are a few simple guides. A positive delta wave in lead V1 indicates a left-sided pathway. A negative delta wave in leads III and aVF together with positive waves in leads V2 and V3 indicates a posteroseptal pathway (Figure 10.7b), while a right free wall pathway is usually associated with positive waves in leads II and III and a negative wave in lead V1.


Jun 4, 2016 | Posted by in CARDIAC SURGERY | Comments Off on Wolff–Parkinson–White Syndrome

Full access? Get Clinical Tree

Get Clinical Tree app for offline access