Agustin Castellanos

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.

His Bundle Recordings in Patients with Reciprocating Tachycardias and Wolff-Parkinson-White Syndrome

The mechanisms of reciprocating tachycardias were studied in three patients with WPW syndrome using the catheter technic of His bundle recordings. In the first case it could not be determined with certainty whether the tachycardias involved two anatomically independent fascicles or a single longitudinally dissociated pathway. They were terminated by carotid sinus pressure, which caused A-V nodal block, or by properly timed atrial stimuli, which interrupted the circuit. Short-lived paroxysms of atrial fibrillation in cases 1 and 2 were most probably related to atrial vulnerability. In case 3 there were three types of QRS complexes in lead II representing (a) exclusive His bundle conduction, (b) simultaneous His and Kent bundle conduction, and (c) coexisting His and infra-nodal preferential (Mahaim fiber[?]) conduction. This patient also had three types of reciprocating tachycardias-two of ventricular, and one of atrial origin. The reciprocating circuit probably involved the three pathways.

His bundle electrograms in two cases of Wolff-Parkinson-White (pre-excitation) syndrome.

The catheter technic for recording the electrical activity of the specialized conducting system in the human heart showed in two patients studied that ventricular pre-excitation was apparently due to a bypass of the His bundle. Intermediate forms of WPW complexes appeared to be combination beats resulting from the activation of the ventricles through impulses traversing both the His bundle and accessory communications. Preferential iatrogenic activation of an intra-atrial (and perhaps even of an atrioventricular) tract appeared to occur in one of the patients. The patients with the WPW (pre-excitation) syndrome and long histories of paroxysmal arrhythmias were successfully treated with a combination of oral propranolol and implanted (transvenous) demand pacemaker.

The Genesis of QRS Changes Produced by Selective Coronary Arteriography

Selective coronary arteriography produces characteristic ST-T changes associated with significant axis shifts. In patients with normal control ÂQRS (mean, +88.6°; SD ± 12.2°) left coronary injections induced an important leftward deviation of the ÂQRS: mean, +8.2°; SD, ±49.1° (P < 0.001). Right coronary artery opacification changed the ÂQRS from a control mean of +66.5°; SD, ±17.2° to a mean of 89.3°; SD, ±16.7° (P < 0.001). Left axis shifts after left coronary artery injections were significantly more marked than right axis deviation after right coronary injections. Important increases (beyond 0.02 sec) in ventricular activation time were not observed. These electrocardiographic abnormalities were attributed to the transient ischemic or toxic effect produced by the bolus of dye. This could result in different degrees of complete or incomplete block in the divisions of the left branch or in an extensive peripheral block affecting large areas of the subendocardial regions of the heart.

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.

Retrograde Activation of the His Bundle During Intermittent Paired Ventricular Stimulation in the Human Heart

Intermittent paired ventricular pacing was performed in five patients, one of them with Wolff-Parkinson-White (WPW) syndrome. Retrograde activation of the His bundle and of the atria was observed in all patients. Bipolar leads with interelectrode distances of 1 mm seemed to be slightly better than the conventional ones (10 mm apart) for the identification of His (H) deflections buried inside the QRS complexes. Diagnosis of retrograde atrial activation was enhanced by the use of a high bipolar right atrial lead. In cases 1 and 2, V2-A2 and V2-H2 intervals consistently lengthened as the V1-V2 interval was reduced. In two other patients, previously present retrograde P waves disappeared as the V1-V2 interval was reduced. Yet at even shorter intervals, retrograde conduction to the His bundle and to the atria was seen. Ventricular echoes occurred in two cases, and reciprocating tachycardia in one. In these instances the His bundle was engaged in both retrograde and forward conduction. Finally in the patient with WPW syndrome A2 preceded H2 at a given coupling interval, suggesting retrograde atrial pre-excitation through an extra-Hisian pathway.

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.