Abdul S. Agha

Factors regulating ventricular rates during atrial flutter and fibrillation in pre-excitation (Wolff-Parkinson-White) syndrome.

known to alternate but the reasons why the ratescould vary so muchhave been a matter of debateandspeculation. Thepresent communicationandaprevious study (Castellanos et al., I973) suggestedthat ventricular rate depended on the duration ofthe effective refractory period of the accessorypathway. When it was longer than that of thenormal AVpathway (and AVnodal block was notpresent) the majority of the impulses were trans-mitted across the normal AVpathwaythrough the

His Bundle Electrograms in Patients with Short P-R Intervals, Narrow QRS Complexes, and Paroxysmal Tachycardias

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 Stimulus1-Stimulus2 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.

Type I, Type II, and Type III Gaps in Bundle-Branch Conduction

“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 H1-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 H1-H2 intervals were shorter and the H2-V2 longer than that at which complete RBBB had been present.In the patient with type III gap and complete LBBB, conduction to the ventricles through the right branch failed at long coupling intervals but was resumed at shorter coupling intervals while the H1-H2 intervals were shorter, and the H2-V2 intervals similar, to those at which block had occurred. True supernormal conduction was excluded in the first two cases. Nevertheless, this phenomenon, as well as a longitudinal dissociation, varying pulsatile vagal discharges acting on an area of depressed conductivity, and phase 4 diastolic depolarization in the right branch coexisting with complete block in the left branch, could have been responsible for type III gap.

Supernormal Conduction in the Human Atria

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 response1-response2 (R1-R2) intervals were shorter than the corresponding St1-St2 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.

Bipolar catheter electrograms for study of retrograde atrial activation pattern in patients without pre-excitation syndromes.

The sequence of retrograde atrial activation of premature ventricular beats was studied in 12 patients without pre-excitation syndrome. Forward and retrograde AV nodal conduction times were within normal limits. The septal low right atrial (LRA2) deflection was inscribed 25 to 55 ms (ave: 37.9 ms) before the low left atrial (LLA2) electrogram and 35 to 75 ms (ave: 53.7 ms) ahead of the high right atrial (HRA2) deflection. LLA2 preceded HRA2 in 8 patients, more or less coincided with HRA2 in 3 cases, and was inscribed 10 ms ahead in 1 patient. In all cases a decrease in the coupling (St1-St2) interval resulted in a proportional increase of the septal LRA1-LRA2, LLA1-LLA2, and HRA1-HRA2 intervals. Atrial echoes occurring in 3 cases had a sequence of arrival of excitation at the recording sites which was similar to the ones shown by the same patients during ventricular pacing. This is in keeping with the existence of an upper common pathway located above the area where functional longitudinal dissociation occurred. Thus, it is concluded that impulses emerging from the AV node in a retrograde direction reach the septal low right atrium before they activate the explored low left atrial sites, regardless as to whether they arise in the ventricles or in the atria.

Double accessory pathways in Wolff Parkinson White syndrome

Intracardiac electrophysiological studies were performed in two patients with Wolff-Parkinson-White (WPW) syndrome. Atrial pacing at increasing rates or shorter coupling intervals produced inscription of the forward His bundle deflection at progressively longer intervals after the onset of ventricular depolarization. There was an associated increase in QRS duration without any change in the P-R (or St-V) interval. This response was consistent with a Kent bundle. Case 1 also had a short A-H interval which did not show the expected prolongation with stimulation at progressively faster rates. This suggested the presence of a James bundle in addition to the Kent bundle. In case 2 beats conducted exclusively through the atrioventricular (A-V) node had a short H-V interval but a delta wave was not inscribed. Absence of an initial slurring was attributed to the existence of an infra-His bundle bypass of the Mahaim type causing only slight pre-excitation, which was not of sufficient magnitude to be recorded by body surface leads. However, the existence of a congenitally short anterosuperior division of the left bundle could nt be excluded.

Wenckebach phenomenon within the atria.

rates ranged between I58 and I94 a minute. This phnomenon (also observed by Lewis, Feil, and Stroud, I918-I920) was manifested by a gradual prolongation of the stimulus-to-atrial electrogram intervals until one stimulus failed to reach the recording electrodes. The localization of the site ofdelay and block could be made exclusivelyfrom the intracardiac recordings, since the surface leads showed what appeared to have been only an AV nodal Wenckebach. In Case 2 the intraand interatrial as well as the atrioventricular conduction patterns were studied during intermittent paired high right atrial pacing. Though this patient had complete right bundle-branch block and left anterior hemiblock, the major area of delay was in the atria. The full recovery period of the latter occurred at a longer StI-St2 interval than that of the AV node or His Purkinje system.

Functional properties of accessory AV pathways during premature atrial stimulation.

Premature atrial stimulation was performed during His bundle recording in four patients with the type of ventricular pre-excitation in which theforward H deflection appeared after the onset of the delta wave. The AV conduction patterns occurring in these patients seemed to have depended on the physiological differences existing between normal pathway and accessory pathway (AP) at different moments of the cycle. These differences explained the patterns noted in driven beats, namely, exclusively accessory pathway conduction (Case i), combined accessory and normal pathway conduction (Case 2), and exclusive normal pathway conduction (Cases 3 and 4). In Cases i and 3 the effective refractory period of the AP was longer than that of the normal pathway. Moreover, Case 3 had AP conduction only towards mid-cycle, sandwiched in between periods of normal pathway conduction. In Case 2, with very short refractory periods (less than I70 msec), premature atrial impulses reached the ventricles during the peak of the T wave. Case 4 had normal pathway conduction with right bundle-branch block in sinus, driven, and late diastolic testing beats, with AP conduction only at the shorter coupling intervals. The ventricular rates of spontaneous or induced atrial tachyarrhythmias were significantly faster when the accessory pathways effective refractory period was short (Cases 2 and 4), than in the other two (Cases i and 3) with longer effective refractory periods. Though premature atrial stimulation has increased our knowledge of AV conduction, more studies are necessary to extend their usefulness to other patients with pre-excitation syndrome.

His bundle recordings in diagnosis of impulse formation in Kent and Mahaim tracts.

His bundle electrograms were recorded in 2 patients with ectopic beats arising in accessory atrioventricular tracts. Case 1 had Wolff-Parkinson-White (WPW) type A and a left-sided Kent tract with a short effective refractory period. Though ectopic impulse formation most probably occurred within the Kent tract itself, a vulnerability-related origin in the ventricular muscle close to the distal end of the Kent tract could not be excluded. In Case 2, with a Mahaim tract extending from His bundle to ventricles, there were three types of QRS morphologies resulting from : (a) atrioventricular conduction exclusively through the normal pathways; (b) atrioventricular conduction through both, normal pathway, and Mahaim tract; and (c) ectopic impulse formation in the Mahim tract. Specialized electrophysiological studies were essential to diagnose these unusual arrhythmias.

Arrival of Excitation at the Right Ventricular Apical Endocardium in Wolff-Parkinson-White Syndrome Type B

His bundle and bipolar right ventricular apex (RVA) and right ventricular outflow tract (RVOT) catheter electrograms taken from sites 1 mm apart were recorded simultaneously with various surface leads in two patients with Wolff-Parkinson-White syndrome (WPW) type B. In “fusion’ beats the presence of a normal H-RVA interval indicated that the apex of the right ventricle was activated by the impulse emerging from the right branch. On the other hand, a shorter-than-normal H-RVA interval implied that the RVA was depolarized by the activation front propagating from the pre-excited site. When this occurred, the V-RVA intervals gave a rough estimate of conduction time from pre-excited area to RVA. The values obtained (40 and 50 msec, respectively) were shorter than in two other patients with WPW type A.The arrival of excitation patterns in the right ventricular endocardium were similar in WPW type B and in beats produced by RVA stimulation but differed markedly from that of left anterior hemiblock even when the surface electrocardiographic leads showed abnormal left axis deviation in all instances. This resemblance between ventricular complexes attributed to WPW type B and those resulting from stimulation of an inferior (apical) site suggests, but does not prove, that the impulses propagated from an equivalent region of the right ventricle. These simultaneously recorded His bundle and right ventricular endocardial electrograms during electrical stimulation of the heart have increased our knowledge of Wolff-Parkinson-White syndrome.