Wolff-Parkinson-White Preexcitation Patterns

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Chapter 12 Wolff-Parkinson-White Preexcitation Patterns

This chapter is a bridge between the first part of the book dealing primarily with abnormal QRS-T patterns and the second part on arrhythmias. Preexcitation patterns, especially the Wolff-Parkinson-White (WPW) pattern, may be mistaken for bundle branch blocks, hypertrophy, or myocardial infarction (MI) and are also an important substrate for supraventricular tachycardias. Even beginning clinicians need to be familiar with this finding, still a relatively common cause of referral to cardiologists.

Wolff-Parkinson-White Pattern: Preexcitation and Bypass Tracts

The WPW pattern is a distinctive and important ECG abnormality caused by preexcitation of the ventricles. Normally the electrical stimulus travels to the ventricles from the atria via the atrioventricular (AV) junction. The physiologic lag of conduction through the AV junction results in the normal PR interval of 0.12 to 0.2 sec. Consider the consequences of having an extra pathway between the atria and ventricles that would bypass the AV junction and preexcite the ventricles. This situation is exactly what occurs with the WPW pattern: an atrioventricular bypass tract connects the atria and ventricles, circumventing the AV junction (Fig. 12-1).

Bypass tracts (also called accessory pathways) represent persistent abnormal connections that form and fail to disappear during fetal development of the heart in certain individuals. These abnormal conduction pathways, composed of bands of heart muscle tissue, are located in the area around the mitral or tricuspid valves (AV rings) or interventricular septum. An AV bypass tract is sometimes referred to as a bundle of Kent.

Preexcitation of the ventricles with the classic WPW pattern produces the following characteristic triad of findings on the ECG (Figs. 12-2 to 12-4):

The QRS complex in sinus rhythm with WPW pattern is the result of the competition (fusion) between signals going down the normal conduction system and down the bypass tract. The signal going down the bypass tract usually reaches the ventricles first, while the signal going down the normal conduction system gets delayed in the AV node. The early activation of the ventricles results in a shorter than normal PR interval. Slow conduction through the ventricular muscle from the bypass tract insertion site is responsible for the initial QRS slurring (delta wave). Once the signal going down the normal conduction system passes the AV node, this activation wave “catches up” with the preexcitation wave by spreading quickly through the His-Purkinje system and activating the rest of the ventricles in the usual way. This competitive mechanism produces the relatively narrow second part of the QRS complex. The degree of preexcitation (amount of the ventricles activated through the bypass tract) therefore is dependent on the speed of AV nodal conduction—the longer the delay in the AV node, the larger portion of the ventricles that is activated through the bypass tract and the longer the delta wave is.

Figures 12-2 and 12-3 show the WPW pattern, with its classic triad of a widened QRS complex , a short PR interval, and a delta wave. Notice that the pattern superficially resembles a bundle branch block pattern because of the widened QRS complexes.

Bypass tracts can be located anywhere along the AV groove and interventricular septum. Some patients have more than one bypass tract.

Very detailed algorithms based on the 12-lead ECG have been proposed to determine the localization of the bypass tract for the purposes of ablation. However, the predictive rules are beyond the needs of most clinicians. Furthermore, the accuracy of these often complex algorithms is limited in the presence of multiple bypass tracts and when preexcitation is more subtle.

If the bypass tract inserts into the lateral part of the left ventricle, the initial QRS vector will point from left to right. Thus, the delta waves will be negative in lead I or aVL and positive in lead V1, resembling a right bundle branch block (RBBB) or high lateral wall MI pattern.

If the bypass tract hooks into the posterior region of the ventricles, the ECG usually shows positive delta waves in most of the precordial leads and negative delta waves in the inferior limb leads (resembling an inferoposterior infarct; see Fig. 12-3).

With right free wall preexcitation, the QRS complexes are predominantly negative in V1 and V2, resembling a left bundle branch block (LBBB). The delta waves are typically byphasic or slightly positive in V1/V2 and positive in V6 (Fig. 12-4). The QRS axis is horizontal or leftward.

Anteroseptal bypass tracts, the rarest WPW variant, may be associated with negative delta waves in leads V1 and V2 (resembling an anteroseptal infarct). The frontal plane axis is more vertical.

More detailed algorithms based on the 12-lead ECG have been proposed to determine the localization of the bypass tract for the purposes of ablation. However, these predictive rules are beyond the needs of most clinicians. Furthermore, their accuracy complex is limited in the presence of multiple bypass tracts and when preexcitation is more subtle.

Clinical Significance

The classic WPW appearance on ECG has been reported in roughly 1 to 2 per 1000 individuals. In some instances, familial occurrence is observed. Right ventricular bypass tracts are sometimes associated with other forms of congenital heart disease, especially Ebstein’s anomaly of the tricuspid valve. Left-sided bypass tracts usually are not associated with structural heart disease.

The major significance of WPW preexcitation is twofold:

1. Individuals with this pattern are prone to arrhythmias, especially paroxysmal supraventricular tachycardia (PSVT) (see Fig. 12-4) and atrial fibrillation. In the latter instance, if the rate becomes extremely fast, atrial fibrillation may lead to ventricular fibrillation with sudden cardiac arrest. Fortunately, this occurrence is very rare. These important topics, introduced briefly in this chapter, are discussed further in Chapters 14 and 20.

2. The WPW ECG is often mistaken for either a bundle branch block, due to the wide QRS, or for an MI, due to the negative delta waves simulating pathologic Q waves (see Fig. 12-3).

The WPW abnormality predisposes patients to develop PSVT because of the presence of the extra conduction pathway. For example, a premature impulse traveling down the AV junction may recycle up the accessory pathway and then back down the AV junction, and so on. This type of recirculating impulse is an example of reentry. The important topic of reentry and PSVT is discussed further in Chapter 14.

When PSVT develops in a patient with the WPW preexcitation pattern, the QRS complex generally becomes narrow (Fig. 12-5). The widened QRS seen with WPW syndrome during normal sinus rhythm occurs because the stimulus travels concomitantly down the bypass tract and down the AV junction, resulting in a type of hybrid or fusion beat. When PSVT occurs, the impulse usually travels down the AV junction and back up the bypass tract in a retrograde fashion, resulting in a loss of the delta wave. (The delta wave and wide QRS will only be seen when an impulse travels down the bypass tract.)

Of note, some patients with bypass tracts do not show the classic WPW pattern during sinus rhythm but may develop reentrant types of PSVT. These patterns associated with a concealed bypass tract are described in Chapter 14.

Another type of preexcitation variant, the Lown-Ganong-Levine (LGL) syndrome, may be caused by a bypass tract that connects the atria and AV junction area. Bypassing the AV node results in a short PR interval (less than 0.12 sec). However, the QRS width is not prolonged, because ventricular activation occurs normally. Therefore the LGL pattern consists of a normal-width QRS complex with a short PR interval and no delta wave. In contrast, the WPW pattern consists of a wide QRS complex with a short PR interval and a delta wave (see Fig. 10-19). Patients with the classic LGL syndrome may also have intermittent reentrant-type PSVT or paroxysmal atrial fibrillation or flutter.

Most people with a short PR interval and normal QRS, however, do not actually have LGL preexcitation. For example, a relatively short PR interval may be seen as a normal variant, without a bypass tract, because of accelerated AV conduction. Therefore, you should not “overread” an ECG on which the only noteworthy finding is a somewhat short PR interval, especially in an asymptomatic person. Such ECGs can be read as “Short PR interval without other evidence of preexcitation,” or as “Short PR interval which may be seen as a physiologic variant (accelerated AV conduction pattern), although a preexcitation variant cannot be excluded.”

Another rare preexcitation variant is related to a slowly conducting bypass tract that typically connects the right atrium with the right bundle branch or right ventricle. These “atriofascicular” or “atrioventricular” fibers are sometimes referred to as Mahaim fibers. The 12-lead ECG in sinus rhythm may be normal or may show a normal PR interval with a subtle delta wave. If PSVT develops, the impulse goes down the bypass tract, stimulates the right ventricle before the left, and then reenters up the AV node. This sequence will produce an LBBB pattern during the tachycardia.

Treatment

Patients with WPW who have symptomatic tachycardias can usually be cured by an ablation procedure during which the bypass tract is ablated using radiofrequency (RF) current. This highly successful treatment requires a cardiac electrophysiologic (EP) procedure in which special catheters are inserted into the heart through peripheral veins and the bypass tract is located by means of ECG recordings (cardiac electrograms) made inside the heart.

Patients who are not candidates for RF catheter ablation therapy can usually be treated with drug therapy.

Not all individuals with the WPW pattern have associated arrhythmias. Occasionally, the WPW pattern will be discovered in asymptomatic subjects who have an ECG ordered as part of a routine examination or for other indications. The major concern is the risk of the sudden onset of atrial fibrillation leading to ventricular fibrillation. Fortunately, the risk of sudden death from this mechanism is extremely low in completely asymptomatic subjects with the WPW patterns. Individuals in whom a WPW pattern is discovered as an incidental finding, therefore, usually do not require specific intervention. Disappearance of the WPW pattern during exercise (with the appearance of a normal QRS with sinus tachycardia) is particularly reassuring. Electrophysiologic evaluation and prophylactic ablation therapy in asymptomatic subjects are sometimes considered in special circumstances, for example, with competitive athletes, pilots, and those with a family history of sudden death.

Overview: Differential Diagnosis of Wide QRS Complex Patterns

Finding a wide QRS complex pattern is of importance because it is often indicative of an important abnormality with significant clinical implications. The major ECG patterns that produce a widened QRS complex can be divided into four major categories.

Differentiation among these four possibilities is usually straightforward. The ECG effects of RBBB and LBBB have already been described in Chapter 7. Hyperkalemia produces widening of the QRS complex, often with loss of P waves (Chapter 12). Widening of the QRS complex in any patient who is taking an antiarrhythmic or a psychotropic agent should always suggest possible drug toxicity. Pacemakers generally produce an LBBB pattern with a pacemaker spike before each QRS complex. (An important exception is biventricular pacing used in the treatment of chronic heart failure (CHF) in which an RBBB pattern is usually seen in conjunction with the left ventricular component of pacing; see Chapter 21.) The WPW pattern is recognized by the triad of a short PR interval, a wide QRS complex, and a delta wave, as discussed in this chapter.