His bundle electrograms were recorded in three patients with short P-R intervals, narrow QRS complexes, and a history of paroxysmal tachycardias. During sinus rhythm or atrial stimulation with long cycle lengths, the shortening of the P-R interval was due to a decrease in the low right atrium-His (LRA-H) interval (representing A-H conduction time). The latter was also short during retrograde (V-A) conduction. These findings support the existence of an A-V nodal bypass operation in both directions. In one patient, the LRA-H interval did not lengthen when the atrial rate was increased. Intermittent atrial pacing was performed in the two other patients. The LRA-H interval was short at long coupling intervals, but it started to increase (progressively) at a given Stimulus 1 -Stimulus 2 interval. Apparently, the refractory period of the accessory bundle was encountered so that the impulse was propagated, with various degrees of delay, through the A-V node. A James bundle need not be present in all patients with similar electrocardiograms. Abnormalities of unknown origin could cause this phenomenon. Reciprocating tachycardias were induced by stimulation of the atria in one patient. The triggering beat consistently had a long A-V conduction time. Although in this case retrograde (V-A) propagation most probably occurred through the accessory communication, the possibility of a functional intranodal dissociation of a single anatomical pathway could not be excluded.

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Gaps" in bundle-branch conduction were observed in three patients using the combined technic of premature atrial stimulation and His bundle recordings.In type I gap a complete LBBB pattern disappeared at shorter coupling intervals because the premature atrial impulses encountered enough delay at the A-V node to reach the left bundle branch after the end of its effective refractory period. When this occurred, the H,-H2 intervals were longer and the H2-V2 intervals shorter than that at which complete LBBB had been present.In type II gap a complete RBBB pattern disappeared at shorter coupling intervals because the premature atrial impulses were so delayed within the proximal His-Purkinje system that they reached the right bundle branch after the end of its effective refractory period. When this occurred the

Premature atrial stimulation and His bundle recordings were performed in 6 patients with pre-excitation (WPW) syndrome. The ventricular rates during bursts of atrialflutter and atrialfibrillation triggered by the earliest impulses depended on the functional properties of the accessory pathway. In 3 patients in whom the effective refractory period of the accessory pathway was longer than that of the normal AV pathway the ventricular rates did not exceed 2IO/min; the majority of the supraventricular impulses reached the ventricles through the normal A V pathway. In 3 other patients in whom the effective refractory period of the accessory pathway was very short (less than 220 msec) the ventricular rates were as high as 3IO/min; the majority of the impulses reached the ventricles through the accessory pathway. Concealed A V conduction occurred in both pathways producing RR pauses well in excess of the duration of the corresponding effective refractory periods. These tachyarrhythmias were due to stimulation during the atrial vulnerable period, not to a reciprocating mechanism involving two separate anatomical AV communications.Intracardiac recordings were necessary to evaluate the A V conduction patterns as well as the nature of the wide QRS complexes seen during the tachyarrhythmias.Factors regulating the ventricular rates during atrial flutter and fibrillation in patients with pre-excitation (WPW) syndrome are not well known. Previous studies from our department suggested that the AV conduction patterns occurring during these tachyarrhythmias depended on the duration of the effective refractory period of the accessory pathway and on its relation to that of the normal pathway (Castellanos et al., 1973).The present communication corroborates these assumptions.

A supernormal period of intra- and interatrial conduction was observed in five patients during premature stimulation of various atrial sites with driving cycle lengths ranging between 500 and 600 msec. Electrograms were recorded with filtered, 1-mm apart, bipolar catheter electrodes placed in the high right atrium, coronary sinus, and midleft atrium. The supernormal period, which lasted from 90 to 140 msec, was located at the end of the relative refractory period. During this part of the cycle, the response 1 -response 2 (R 1 -R 2 ) intervals were shorter than the corresponding St 1 -St 2 intervals. As in experiments performed with plunge electrodes, the conduction time of premature atrial responses was shorter than in late diastolic or driven beats. Although a mechanical origin (due to inevitable catheter movement produced with cardiac motion) can be invoked in the genesis of these changes, it is highly probable that supernormality was a true electrophysiologic event involving, predominantly, the specialized atrial tracts.