The Role of Premature Beats in the Initiation and the Termination of Supraventricular Tachycardia in the Wolff-Parkinson-White Syndrome

In four patients with WPW syndrome atrial and ventricular premature beats were induced and the changes in form of the ventricular and atrial complexes were studied. Results indicate that, depending upon the timing of the premature atrial beat and the state of refractoriness of the His and Kent bundles, excitation of the ventricles occurs predominantly through the atrioventricular nodal system, predominantly through the Kent bundle or exclusively through one or both conduction systems. With short delays conduction through the Kent bundle may be blocked and only normal excitation of the ventricles occurs. In one patient with a history of attacks of tachycardia these normal QRS complexes were followed by retrograde activation of the atria by the Kent bundle, and attacks of supraventricular tachycardia of shorter or larger duration occurred. They stopped spontaneously, sometimes by delay or block, either of retrograde Kent conduction or of antegrade A-V nodal conduction, making it possible for the sinus node to capture the ventricles. They also could be terminated by induced atrial premature beats. In two patients tachycardias could be induced by appropriately timed ventricular premature beats during regular driving of the right ventricle. In one of these patients a circus movement, involving the Kent bundle, is probably present. By appropriate stimulation of the atria or ventricles during an attack of supraventricular tachycardia in this patient, one cycle length could be shortened without changing those of the following beats. These results suggest that a circus movement involving the atria, the normal atrioventricular conduction system and the Kent bundle is present. In the other patient, not fulfilling the WPW criteria, ventricular or atrial premature beats did not interfere with the basic rhythm of the tachycardia. Two hypotheses for this tachycardia are given: nodal tachycardia caused by rapid firing of the A-V node or a nodal tachycardia caused by a reciprocal mechanism in the A-V junction. The attacks could be blocked too by appropriately timed atrial and ventricular premature beats. No ventricular type of tachycardia could be demonstrated.