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Atrioventricular (AV) Conduction Disorders, Part II: Preexcitation (Wolff–Parkinson–White) Patterns and Syndromes


The previous chapter focused primarily on disorders associated with delays in atrioventricular (AV) conduction, termed AV heart blocks. This chapter describes an entirely different class of AV conduction disorders, namely those related to abnormally early ventricular excitation ( preexcitation ). Our specific focus will be their most common presentations, namely Wolff–Parkinson–White (WPW) patterns and associated arrhythmia/conduction syndromes. This chapter also serves as an extension of the discussion of reentrant supraventricular tachycardias started in Chapter 14 . A notable paradox is that both early ventricular excitation (preexcitation) and delayed ventricular excitation (as with bundle branch blocks and related intraventricular conduction disturbances, described in Chapter 8 ) lead to a widened QRS complex. Another counterintuitive finding is that the classic ECGs of patients in sinus rhythm with a WPW pattern show a wide QRS, whereas when the characteristic reentrant type of paroxysmal tachycardia develops, the ECGs most often show a QRS of normal morphology and duration.

Preexcitation via AV Bypass Tracts

The normal electrical stimulus (signal) generated by the sinoatrial (SA) node pacemaker travels to the ventricles via the atria and AV junction. The physiologic lag in conduction through the AV junction, which allows the ventricles time to fill, results in the normal PR interval (delay time) of 120 to 200 msec. Now consider the consequences of having an extra pathway between the atria and ventricles that provides an alternative means of activating the ventricles. This extra pathway (akin to a short cut or short circuit) would literally bypass the AV junction, and in doing so, allow for early depolarization (preexcitation) of the ventricles. This situation is exactly what underlies the WPW pattern: a functioning AV bypass trac t connects the atria and ventricles, partly or fully circumventing conduction through the AV junction, where the normal, physiologic delay in ventricular activation occurs ( Fig. 18.1 ).

Fig. 18.1, Schematic of electroanatomy underlying the Wolff–Parkinson–White (WPW) preexcitation pattern. A small percentage of individuals are born with an accessory fiber (atrioventricular bypass tract) connecting the atria and ventricles.

Bypass tracts (also called accessory or anomalous pathways ) represent persistent abnormal connections that form and fail to disappear during fetal development of the heart (but may stop conducting during later life). These abnormal conduction pathways, composed of short bands of heart muscle tissue, are usually located in the area around the mitral or tricuspid valves (AV rings) or interventricular septum. An AV bypass tract is sometimes referred to, historically, as a bundle of Kent. A number of rarer forms of accessory connections exist, as briefly discussed in the following sections.

The Classic WPW Triad

Preexcitation of the ventricle during sinus rhythm with its classic triad signature produces the WPW signature ( Figs. 18.2–18.4 ):

  • 1.

    The PR interval is shortened (often but not always to less than 120 msec) because of the ventricular preexcitation.

  • 2.

    The QRS complex is widened, giving the superficial appearance of a bundle branch block pattern. However, the wide QRS is caused not by a delay in ventricular depolarization but by early stimulation of the ventricles. Furthermore, the T wave is usually opposite in polarity to the wide QRS in any lead, similar to what is seen with bundle branch blocks (another example of “secondary T wave inversions”).

  • 3.

    The upstroke of the QRS complex is slurred or notched. This notching, called a delta wave, results from relatively slow conduction through the ventricular muscle, itself, at the bypass tract insertion site, compared with more rapid conduction within the His-Purkinje system.

Fig. 18.2, Preexcitation via the bypass tract in the WPW pattern is associated with a triad of findings.

Fig. 18.3, Notice the characteristic triad of the WPW pattern: 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 V 2 to V 6 ) and widened QRS complexes. The Q waves in leads II, III, and aVF are 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 region of the ventricles (possibly posteroseptal in this case).

Fig. 18.4, Another example of the WPW pattern 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 V 1 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 QRS Complex as a Fusion Beat in WPW

The QRS complex in sinus rhythm with WPW pattern, therefore, can be viewed as the result of a competition (race) involving two sets of signals, one going down the normal AV conduction system and the other down the (accessory) AV bypass tract. The signal going down the bypass tract usually reaches the ventricles first, while the signal going down the normal conduction system is delayed in the AV node. 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 stimulating the rest of the ventricles in the usual way. Thus the degree of preexcitation (amount of ventricular activation through the bypass tract) is dependent on the relative speeds of AV nodal versus bypass tract conduction. Accordingly, the greater the relative delay in the AV node, the larger the portion of the ventricles that is activated through the bypass tract, and the more apparent the delta wave will be. The QRS complex in WPW, therefore, can be viewed as a kind of fusion complex, resulting from the contribution of depolarization via the normal AV nodal pathway and that via the accessory pathway.

Anomalous activation of the ventricles via a bypass tract can lead not only to certain arrhythmias but also to QRS alterations mimicking bundle branch blocks, hypertrophy, or infarction, as well as to secondary ST-T changes simulating ischemia. Figs. 18.2 and 18.3 show the WPW pattern, with its classic triad of a short PR interval, a widened QRS complex, and a delta wave.

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