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Various electrocardiographic and vectorcardiographic (ECG-VCG) patterns of ventricular conduction disturbances are inducible by premature right atrial stimulation (PRAS). These patterns are a consequence of different degrees of refractoriness in the specialized ventricular conduction system. We observed that the intermediate phase of left bundle branch block (LBBB) induced by PRAS in 20 subjects with normal basal QRS (complexes) were similar to those of left ventricular hypertrophy (LVH). In 18 patients with basal ECG-VCG signs of LVH, right bundle branch block (RBBB) induced by PRAS produced a progressive disappearance of these signs and the "normalization" of the tracings. The initial maximum QRS vector decreased, disappeared or remained absent in the patients with LBBB induced by PRAS, and appeared (when absent in the basal VCG) and remained unchanged (when present) in patients with RBBB induced by PRAS. In this paper we discuss the electrogenetic implications of these data. The ECG-VCG sings of LVH are probably dependent on a slowed conduction in the left bundle branch system, while anatomical hypertrophy per se probably plays a less important role.

Anterior displacement (AD) of the QRS horizontal loop (Frank VCG method) was induced by programmed right atrial stimulation (PRAS) in 15 cases. When AD occurred we noticed changes of the terminal QRS vectors and of the T loop similar to those observed in incomplete right bundle branch block (RBBB). The increasingly anticipated extrastimuli induced progressively the AD and then progressive degrees of RBBB. The anterior shifting of the efferent limb never appeared after the induction of RBBB. A left conduction disturbance never appeared after the AD. In cases of supposed incomplete left bundle branch block (i.e. left ventricular hypertrophy) the QRS duration decreased when the AD was induced. Therefore, the AD induced by PRAS and probably those observed in some clinical cases are due to a right ventricular conduction disturbance.

Recently a unique clinical entity has been suggested in subjects without apparent heart disease presenting with recurrent ventricular tachycardia (VT) characterized by RBBB + LAH electrocardiographic pattern, relatively slow rate, induction by atrial stimulation, and interruption by verapamil. According to these characteristics, three cases (2 M and 1 F, aged 18, 33 and 66 years) are presented in this study. They have had palpitations from one to twenty years, but not syncopal episodes. During VT the cycle length ranged from 300 to 480 msec. VT was terminated both by verapamil and by ajmaline. VT was inducible in 3/3 cases by incremental atrial pacing when cycle length of pacing became similar to that of spontaneous VT; in 2/3 cases VT was induced by programmed right atrial stimulation and in 2/3 cases by programmed ventricular stimulation. Serial electrophysiological studies for pharmacological and therapeutic evaluation applied to 1/3 cases showed: amiodarone given orally (200 mg/die) for two months prevented the induction of VT while verapamil, propranolol, mexiletine, and propafenone tested intravenously were ineffective. In the remaining two patients amiodarone, tested only intravenously, was not effective to prevent the induction of VT but lengthened its cycle length. All patients received amiodarone orally (200 mg/die) and were followed for 2,7 and 8 years respectively. Two of them had no more episodes of VT and one, while asymptomatic, continued to present with. The electrophysiological mechanism of this form of VT cannot be identified with certainty, but many data suggest a reentry in the posterior fascicle of left bundle branch as the most probable mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Although in the last years very important knowledges have been obtained in the field of the intraventricular conduction disturbances, many electrocardiographic-vectorcardiographic findings concerning the left bundle branch block (LBBB) and their electrogenesis are still controversial. With the purpose to clarify this problem we have reviewed and analysed 23 cases in whom BCG-VCG patterns of "complete" or "incomplete" LBBB were induced by the premature right atrial stimulation (PRAS) during an electrophysiologic study in man. The analysis of these cases have demonstrated that: 1) the same LBBB pattern can be caused by a slowed conduction or block at different sites of left intraventricular conduction system i.e. not only in the main stem of the left bundle branch (LBB) (tronkular LBBB) but also within the bundle of His (intra-His LBBB) or in all the three fascicles of the LBB distally to its subdivision (divisional LBBB); 2) ECG-VCG are not able to distinguish the anatomical or functional site of slowed conduction or block; 3) the right or left axis deviation in the LBBB is not due to LBBB per se but it represents or a block at two different sites, i.e. a tronkular or intra His LBBB plus a block in the anterior or posterior subdivision of the LBB, or a block at only one side i.e. a tronkular, intra-His or divisional LBBB but with prevalent involvement of one fascicle of the LBB; 4) the ECG-VCG "incomplete" LBBB pattern is similar to that of the left ventricular enlargement; 5) figures of "atypical LBBB" are not specific of myocardial necrosis; 6) the criteria for the diagnosis of "complete" LBBB are not reliable. We conclude that, since LBBB pattern does not always correspond to a slowed conduction or block in the main stem of the LBB, the current terminology of LBBB is inappropriate and could be changed with another which considers the site of delayed activation and not the site of slowed conduction. Therefore we propose the following terminology: 1) generalized left ventricular activation delay instead of LBBB without axis deviation; 2) generalized left ventricular activation delay superiorly predominant instead of LBBB with left axis deviation; 3) generalized left ventricular activation delay inferiorly predominant instead of LBBB with right axis deviation.