Bradycardia-dependent Bundle Branch Block Research Articles

Aberrant Ventricular Conduction: Revisiting an Old Concept.

The well-defined concept of aberrant ventricular conduction was introduced over 100 years ago and, despite advances in cardiac physiology and electrophysiologic testing, it is still widely misunderstood. Aberrant ventricular conduction is due to physiologic refractoriness of the His-Purkinje system and in most cases does not reflect underlying conduction system disease. Electrophysiologically, aberrant ventricular conduction can manifest with premature atrial ectopics, the Ashman phenomenon with atrial tachyarrhythmias, concealed conduction, echo beats and with the sinus mechanism including rate dependent bundle branch block, bradycardia dependent bundle branch block and early sinus beats. It is important to recognise aberrant ventricular conduction in the context of a broad complex tachycardia, as the differentiation between supraventricular tachyarrhythmias with aberrant ventricular conduction and ventricular tachyarrhythmias carry different therapeutic and prognostic implications. This review will define the ECG footprints of aberrant ventricular conduction to allow accurate ECG interpretation.

Apparent bradycardia-dependent right bundle branch block associated with atypical atrioventricular wenckebach periodicity as a possible mechanism

The Holter monitor electrocardiogram was taken from a 15-year-old male athlete. Intermittent right bundle branch block frequently occurred at rest. When sinus cycles gradually lengthened, sinus impulses were conducted to the ventricles with right bundle branch block (RBBB) in succession. When, thereafter, sinus cycles gradually shortened, sinus impulses were conducted without RBBB. However, it seems that these findings do not show true bradycardia-dependent RBBB. Atypical atrioventricular Wenckebach periodicity was occasionally found in which sudden shift from the period of comparatively short PR intervals to the period of long PR intervals occurred. In the Wenckebach periodicity, when a QRS complex occurs after a much longer pause, RBBB was not found, while when it occurs after a much shorter period, RBBB was found. This suggests that this case may be apparent bradycardia-dependent RBBB, namely, a form of tachycardia-dependent RBBB. This is the first report suggesting apparent bradycardia-dependent bundle branch block associated with gradual lengthening of sinus cycles, as a possible mechanism.

Tachycardia- and bradycardia-dependent left bundle branch block associated with first degree a-v block. A study using his bundle electrogram during carotid sinus compression.

His bundle electrographic examination was performed during carotid sinus compression as well as atrial pacing in a patient who exhibited intermittent left bundle branch block (LBBB) and first degree A-V block. LBBB was observed at the corrected RR intervals below 920 msec and above 1600 msec. The QRS complexes showed normal intraventricular conduction between these 2 values. The critical cycle lengths could not be determined when ordinary RR intervals were used. The HQ interval remained constant at 70 msec regardless of the pattern of intraventricular condution. It was demonsrated that the patient had both tachycardia- and bradycardia-dependent LBBB with first degree A-V block due to HV block. The authors believe this to be the first case of tachycardia- and bradycardia-dependent bundle branch block studied by His bundle electrography. The important role of His bundle recordings and carotid sinus compression in the diagnosis of rate dependent intraventricular conduction disturbance was stressed and possible mechanisms underlying this rare condition were discussed.

Concealed intraventricular conduction in the human heart.

Concealed intraventricular conduction is defined and the following classification of the manifestations of concealed conduction into the bundle branch system is proposed. 1. Trans-septal retrograde concealed intraventricular conduction responsible for (a) perpetuation of functional bundle branch block initiated by a premature supraventriculra impluse; (b) alternation of aberrant ventricular conduction in supraventricular bigeminy; (c) normalization of intraventricular conduction with acceleration or rate in bradycardia-dependent bundle branch block, and (d) prevention of the manifestation of Wenchbach periods of conduction in a bundle branch or fascicle. 2. Antegrade concealed intraventricular conduction responsible for (a) prevention of expected aberrant ventricular conduction when a short cycle follows a long one, and (b) exceptions to the "rule of bigeminy". 3. Retrograde concealed intraventricular conduction of a ventricular escape in association with unidirectional bundle branch or fasciular block responsible for (a) resumption of AV conduction in "paroxysmal AV block" with bundle branch block, and (b) facilitation (due to supernormality) of conduction in type II AV block due to bilateral bundle branch block. 4. Concealed intraventricular conduction of a premature ventricular impulse responsible for (a) initiation or termination of a re-entrant ventricular tachycardia; (b) resetting of an idioventricular pacemaker, and (c) pseudo-intraventricular or pseudo-AV block.

The Mechanism of Intermittent Bundle Branch Block: Relationship to Prolonged Recovery, Hypopolarization and Spontaneous Diastolic Depolarization

Fourteen cases of intermittent bundle branch block (BBB) are reported, in which block was shown to occur both at rapid and slow rates, with an intermediate normal conduction range. Tachycardia-dependent BBB was related to prolonged recovery and was termed “phase-3 block;” bradycardia-dependent BBB was related to hypopolarization plus spontaneous diastolic depolarization (SDD), and was termed “phase-4 block.” Two critical rates do exist; one, separating phase-3 block from normal conduction; the other, separating normal conduction from phase-4 block. The range of normal conduction seems to be inversely related to the amount of injury. It may be extremely narrow when recovery is greatly prolonged, and/or when hypopolarization is severe, and/or when SDD is enhanced. This may simulate supernormality. In other patients, or in the same patient, the normal conduction range may widen up to several seconds, at the expense of both phase-3 and phase-4 block (accordion-like effect). Deeply inverted T waves correlated well with phase-3 and phase-4 block. Bayley’s theory of conventional myocardial injury applies remarkably well to the analysis of injury of the intraventricular conducting fascicles. The only difference is that SDD plays an important additional role in the conduction system.

Editorial Expression

It has been known that an ineffective stimulus of a failing electronic pacemaker can prevent cardiac stimulation by a well functioning demand pacemaker if the rate of the former exceeds that of the latter. A related phenomenon is described for the first time by Massumi and associates—postponement of the demand pacemaker stimulus by an ineffective spontaneous ventricular impulse, a ventricular premature impulse which does not yield a QRS complex, a “concealed ventricular premature systole.” The interest of their observation goes far beyond its practical significance (avoidance of an erroneous diagnosis of pacemaker malfunction) because it lends strong support to Schamroth and Marriott's hypothetical concept of “concealed ventricular extrasystoles.” Finally, this report recalls the concept of concealed ventricular escape beats, “embryonic escapes,” whose phase-4 depolarization is held responsible for conduction delay or block of supraventricular impulses (Singer et al: Circ Res 21:537, 1967) and has been postulated to account for bradycardia-dependent bundle branch block (Massumi: Circulation 38:1066, 1968) and bradycardia-dependent atrioventricular block (Coumel et al: J Electrocardiol 4:168, 1971).

Bradycardia-dependent bundle branch block: Relation to supernormal conduction and phase 4 depolarization

An electrocardiogram is presented in which spontaneous conversion of 2:1 block with first degree block and incomplete left bundle branch block resulted in 3:2 block with normal conduction of the QRS complex after the short R-R interval. Alternation of rate and block with every second beat is a variation of previously described bradycardia-dependent bundle branch block. Phase 4 depolarization and supernormal conduction are inseparable concepts, and both may play a causal role in bradycardia-dependent bundle branch block. Criteria for recognition of this type of block should not disqualify cases in which supernormal conduction may be present, particularly since proximity of the QRS interval to the preceding T wave may not be an adequate test for supernormal conduction in clinical situations. A knowledge of phase 3 and phase 4 events allows one to relate different types of clinical aberrance, from premature aberrance through early beat “normalization,” as in bradycardia-dependent bundle branch block, to normal rate aberrance as in typical bundle branch block and, finally, to escape beat aberrance.

Bradycardia-dependent bundle-branch block. A critique and proposed criteria.

Four cases of bundle-branch block (BBB) occurring with slow heart rates in patients with heart disease are presented. Recognition of bradycardia-dependent BBB is often difficult, and its differentiation from ventricular escape mechanism and from bilateral BBB requires careful analysis. A set of five criteria based on our own observations is presented with a review of the literature. The responsible mechanism for this seemingly paradoxical situation is not known. However, spontaneous depolarization of one or the other of the bundle branches in late stages of diastole appears to be the most plausible explanation.