The ventricular complex observed in WPW syndrome during periods of sinus rhythm is the result of fusion, with intial phase of ventricular activation representing excitation via accessory pathway and later forces produced by excitation of residual portions of ventricle via normal His-purkinje system. The variations in QRS aberrancy in WPW syndrome depend on varying degree of preexcitation.

This experimental study was undertaken to increase our knowledge on the ventricular fusion in WPW syndrome through epicardial mapping after experimental induction of ventricular preexcitaion of WPW type.

In 5 normal dogs, the heart was widely exposed through transverse thoracotomy and positioned in a pericardial cradle, then electric wires were fixed on the epicardium of right atrium and ventricular bases(anterobasal and posterobasal) areas of right ventricle, anterobasal and poaterobasal areas of left ventricle for atrial and ventricular pacing. Epicardial mapping was then performed during atrial pacing alone and during atrioventricular sequential pacing at the same rate. Atrioventricular sequential pacing was done with various short AV intervals(60-110 msec) for the purpose of premature stimulation on ventricular base.

In mapping we used the grid system which consisted of 29 areas to cover the right ventricle and 23 areas to cover the left ventricle. We drew 9 epicardial ishochrone maps in 5 dogs. The epicardial data during atrio-ventriclar sequential pacing were then compared with those during atrial pacing at an identical rate to study the ventricular fusion in WPW syndrome.

The results were as follows;

1) The preexciting wave spread radially from the stimulated basal area to the right and left(or anterior and posterior wall) and the apex.

2) Preexciting wavefronts collided with the normal wavefronts in a wide range of ventricular activation time.

3) Preexcitation widened according to the degree of the shortening of the AV interval.

4) The duration of ventricular activation was greater in preexcited ventricles than in normally activated ventricles. The more prematurely the ventricle was stimulated, the greater the duration of ventricular activation was.