Preexcitation Syndromes

Preexcitation occurs when the ventricles are activated by an impulse from the atria sooner than would be expected if the impulse were transmitted down the normal conducting pathway (the AV node). Several different forms of preexcitation have been described, based on anatomic, clinical, electrocardiographic, and electrophysiologic abnormalities. All forms of preexcitation are felt to be due to accessory tracts that bypass all or part of the normal conducting system. These bypass tracts have specific names (Fig. 2.4:38).

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FIG. 24-38. Anatomic sites of bypass tracts.

James fibers (atriohisian connection) are a continuation of the posterior internodal tract and connect the atrium and proximal His bundle. Atrial impulses can therefore completely bypass the AV node to activate the ventricles. On ECG, this appears as (1) a short PR interval because the usual delay in the AV node is bypassed and (2) a normal QRS because James fibers insert directly into the infranodal conducting system and the ventricles are activated normally. When this is associated with reentrant SVT, the clinical condition is termed the Lown-Ganong-Levine (LGL) syndrome.

Mahaim bundles are composed of myogenic tissue; they originate from either the AV node, His bundle, or bundle branches and insert into the ventricles in the septal region. Atrial impulses pass through the AV node but then bypass all or part of the infranodal conducting system to activate the ventricles. Ventricular activation then occurs from two sources, the bypass tract and the normal conducting system, and the QRS complex represents a fusion of the two. The initial depolarization starts at the ventricular insertion of the bypass tract and is spread slowly by cell-to-cell transmission of the impulse. Subsequent depolarization by way of the faster normal conducting system then overtakes the initial depolarization and activates the bulk of ventricular myocardium. The QRS complex is basically normal with a slurred and distorted initial portion termed a delta wave. On ECG, this appears as a normal PR interval, and an initial distortion of ventricular depolarization (delta wave).

Kent bundles are composed of myogenic tissue and directly link the atria to the ventricles, completely bypassing the AV node and infranodal system. This is the most common form of preexcitation and is the anatomic basis for the Wolff-Parkinson-White (WPW) syndrome. On ECG, this appears as a shortened PR interval and with an initial distortion of ventricular activation (delta wave). Sometimes the bypass tract does not conduct an atrial impulse in the antegrade direction and the QRS complex is entirely normal. However, these concealed bypass tracts may conduct retrograde and be able to sustain reentrant SVT.

The WPW syndrome has been divided into types, depending on the direction of the initial delta wave on the surface ECG. This, in turn, is determined by where the bypass tract (bundle of Kent) inserts into the ventricles and which portion of the ventricles is activated first. In reality, accessory tracts can insert anywhere around the AV annulus; the three types are just the most common locations.

In type A WPW, ventricular activation first occurs in the inferior-posterior region of the left ventricle and the delta wave is directed anteriorly. A positive initial deflection with a dominant R wave is seen in lead V1. Q waves in leads II, III, and aVF are common (Fig.,24-39).

FIG. 24-39. Type A Wolff-Parkinson-White syndrome.

In type B WPW, ventricular activation first occurs in the inferior-posterior region of the right ventricle and the delta wave is directed posteriorly and to the left. A negative initial deflection and rS or QS pattern are seen in lead V 1 (Hg.J.zlQ).

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FIG. 24-40. Type B Wolff-Parkinson-White syndrome.

In type C WPW, ventricular activation first occurs in the posterior-lateral region of the left ventricle and the delta wave is directed to the right, superiorly, and anteriorly. A positive delta wave is seen in lead V-,, with a negative or isoelectric delta wave in leads V5 and V6.

Because there is altered depolarization, repolarization is often abnormal, with changes in the ST segments and T waves. The ECG changes of WPW may mimic changes seen with myocardial ischemia, infarction, or ventricular hypertrophy. Type A WPW may imitate as a posterior MI, and type B WPW may imitate an inferior MI.

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