Clinical Electrocardiography: A Simplified Approach, 7th Edition (2006)


Chapter 12. Wolff-Parkinson-White Preexcitation Patterns

The Wolff-Parkinson-White (WPW) preexcitation pattern is a distinctive and important ECG abnormality caused by preexcitation of the ventricles. Normally, the electrical stimulus passes 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 second. Consider the consequences of having an extra pathway between the atria and ventricles that would bypass or short-circuit 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 ).

FIGURE 12-1  Anatomy of the ECG pattern of the Wolff-Parkinson-White (WPW) preexcitation pattern. In a small percentage of people, an accessory fiber (atrioventricular bypass tract) connects the atria and ventricles. (The consequences of this abnormal, extra conduction path are discussed in the text.)

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 atrioventricular 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 [2] [3] [4]).):



The QRS is widened, giving the superficial appearance of a bundle branch block pattern. The wide QRS is caused, however, not by a delay in ventricular depolarization but by early stimulation of the ventricles. (The QRS is widened to the degree that the PR is shortened.)



The PR is shortened (often but not always to less than 0.12 second) because of the ventricular preexcitation.



The upstroke of the QRS complex is slurred or notched. This is called a delta wave.

FIGURE 12-2  Preexcitation via the bypass tract in the Wolff-Parkinson-White (WPW) pattern is associated with a triad of findings.

FIGURE 12-3  Notice the characteristic triad of the WPW pattern: wide QRS complexes, short PR intervals, and delta waves (arrows) that are negative in some leads (e.g., II, III, and aVR) and positive in others (aVL and V2 to V6). The Q waves in leads II, III, and aVFare the result of abnormal ventricular conduction (negative delta waves) rather than an inferior myocardial infarction. This pattern is consistent with a bypass tract inserting into the posterior wall of the left ventricle.

FIGURE 12-4  Another example of WPW with the triad of wide QRS complexes, short PR intervals, and delta waves (arrows). The finding of delta waves that are predominantly negative in lead V1 and positive in the lateral leads is consistent with a bypass tract inserting into the free wall of the right ventricle. This pattern simulates a left bundle branch block pattern.

The bypass tract initially activates the ventricular myocardium, rather than the faster-conducting specialized (His-Purkinje) system in the ventricles. This early myocardial conduction imparts the distinctive notching or slurring (delta wave) to the very beginning of the QRS.

Figures 12-2 and 12-3 [2] [3] show the WPW pattern, with its classic triad of a widened QRS, 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 on the left lateral, posterior (septal or left ventricular), right free wall, or anteroseptal regions of the ventricles. The most common locations are left lateral and posterior. Some patients have more than one bypass tract. Depending on which area of the ventricles (left or right side) is preexcited first, the ECG may show a pattern simulating that of either RBBB with tall R waves in the right chest leads or LBBB with a predominantly negative QRS in leads V1and V2.

The 12-lead ECG with sinus rhythm may also provide important clues about the specific location of the bypass tract. With reasonable accuracy, you can often predict the insertion point of the bypass tract in the ventricles based on the polarity of the delta wave. As a general rule: the initial QRS complex (delta wave) vector will point away from the area of the ventricles that is first to be stimulated by the bypass tract.

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 leads I and/or aVL and positive in lead V1 (resembling a lateral wall MI pattern).

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

With right free wall preexcitation, the QRS complexes are predominantly negative in V1 and V2 and the delta waves are typically positive in leads 1 and V6 (see Fig. 12-4 ).

Anteroseptal bypass tracts may be associated with negative delta waves in leads V1 and V2 (resembling an anteroseptal infarct).


Estimates of the frequency of this pattern in the general population vary widely, but the classic WPW appearance on ECG has been reported in roughly 1 to 2 per 1000 individuals. In some instances, familial occurrence is observed.

The significance of WPW preexcitation is twofold:



Individuals with this pattern are prone to arrhythmias, especially paroxysmal supraventricular tachycardia (PSVT) (see Fig. 12-4 ). Less commonly, they may also develop atrial fibrillation with a rapid ventricular rate. 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 . Note on terminology: Use the term WPW syndrome to apply to patients with the WPW pattern who also have arrhythmias related to the bypass tract.



The WPW pattern 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 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 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.)

FIGURE 12-5  Conduction during sinus rhythm in the normal heart (top) spreads from the sinoatrial (SA) node to the atrioventricular (AV) node and then down the bundle branches. The jagged line indicates physiologic slowing of conduction in the AV node. With the WPW syndrome (bottom left), an abnormal accessory conduction pathway called a bypass tract (BT) connects the atria and ventricles. With WPW, during sinus rhythm, the electrical impulse is conducted quickly down the bypass tract, preexciting the ventricles before the impulse arrives via the AV node. Consequently, the PR interval is short and the QRS complex is wide, with slurring at its onset (delta wave). WPW predisposes patients to develop an atrioventricular reentrant tachycardia (AVRT) (bottom right) in which a premature atrial beat may spread down the normal pathway to the ventricles, travel back up the bypass tract, and recirculate down the AV node again. This reentrant loop can repeat itself over and over, resulting in a tachycardia. Notice the normal QRS complex and often negative P wave in lead II during this type of bypass-tract tachycardia (see Chapter 14 ).

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 second). The QRS width is not prolonged, however, 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 Figs. 12-2 to 12-4 [2] [3] [4]).

Patients with the classic LGL syndrome 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 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 relatively 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 show a normal PR 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 a left bundle branch block pattern during the tachycardia.


Patients with WPW who have symptomatic tachycardias can usually be cured by a procedure during which the bypass tract is ablated using radiofrequency (RF) current. This highly successful treatment requires a cardiac electrophysiology (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. Sometimes, 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 pattern. Individuals in whom WPW 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 is sometimes considered in special circumstances, for example, with competitive athletes, pilots, and those with a family history of sudden death.



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.



Bundle branch blocks (intrinsic conduction delays) including the classic RBBB and LBBB patterns



“Toxic” conduction delays caused by some extrinsic factor, such as hyperkalemia or drugs (e.g., quinidine, propafenone, flecainide, and other related antiarrhythmics, as well as phenothiazines and tricyclic antidepressants)



Beats arising in the ventricles, which may be ventricular escape beats or ventricular premature beats ( Chapter 16 ), or electronic ventricular pacemaker beats ( Chapters 7 and 21 )



WPW-type preexcitation patterns

Differentiation among these 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 10 ). 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 congestive heart failure 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.



The Wolff-Parkinson-White (WPW) pattern is due to ventricular preexcitation from a bypass tract (accessory pathway) that connects the atria and ventricles, short-circuiting the AV node. As a result, the ECG shows a characteristic triad of findings consisting of (1) a short PR interval, (2) a wide QRS, and (3) slurring or notching of the initial part of the QRS, referred to as a delta wave.

Patients with the WPW pattern are particularly prone to attacks of reentrant-type paroxysmal supraventricular tachycardia (PSVT) that may cause palpitations, shortness of breath, or even syncope.

Less commonly, WPW may be associated with atrial fibrillation with a fast ventricular rate. If the rate becomes very rapid, atrial fibrillation may lead to ventricular fibrillation with sudden cardiac arrest.

The syndrome of symptomatic WPW is curable in most cases by radiofrequency catheter ablation of the accessory pathway during a cardiac electrophysiology procedure.

The differential diagnosis of ECG patterns with a wide QRS complex includes four major classes of abnormalities:



Right or left bundle branch block



“Toxic” conduction delays caused by hyperkalemia or certain drugs



Beats arising in the ventricles, such as ventricular premature beats or pacemaker beats



WPW preexcitation





What caused the wide QRS complex in the ECG shown below?




Right bundle branch block



Tricyclic antidepressant toxicity



Posterolateral MI



Wolff-Parkinson-White preexcitation pattern