Tachycardia-dependent Bundle Branch Block Research Articles

A Case Report of Tachycardia-Dependent Right Bundle Branch Block During Cardiac Resynchronization Therapy

Cardiac resynchronization therapy (CRT) has been shown to improve symptoms and mortality in a suitably selected population with systolic heart failure and prolonged QRS duration. Various factors have been reported to be associated with poor response to CRT. A 67-year-old man with CRT implantation experienced response, nonresponse, and response in turn. The new-onset right tachycardia-dependent bundle branch block was considered to be an exclusive cause. More attention should be paid to the possible changes of paced-QRS morphology, resulting from tachycardia-dependent aberrancy during CRT, ensuring a high percentage of effective biventricular pacing.

Bundle branch block on alternate beats during atrial fibrillation

This article reports a case of tachycardia-dependent right bundle branch block (RBBB) occurring during atrial fibrillation. In some sections of the recording, an alternans occurs between complexes with a complete RBBB pattern and complexes showing normal intraventricular conduction or incomplete RBBB. Alternans is frequently observed during phases of fast and nearly regular rhythm, but it occurs even in the presence of a markedly irregular ventricular response. The RBBB alternans associated with short and regular RR intervals is likely to represent a manifestation of 2:1 bundle branch supernormal conduction, whereas alternans occurring with irregular cycles expresses a complex interaction between the RR cycle length and some mechanisms affecting intraventricular conduction, such as tachycardia-dependent bundle branch block, supernormal conduction and concealed retrograde activation of the anterogradely blocked bundle branch (the so-called “linking” phenomenon).

Overdrive prolongation of refractoriness and fatigue in the early stages of human bundle branch disease

Objectives. The aim of this study was to assess the response of refractoriness in normal and diseased human bundle branches to changes in cycle length, as well as during a long period of continuous overdrive pacing.Background. The anterograde refractory period of the bundle branches in patients with functional bundle branch block shortens as the rate is increased. The rate-dependent response of refractoriness in diseased bundle branches is quite different. However, this difference has not been precisely delineated, and its physiologic meaning is uncertain.Methods. Refractoriness of the bundle branches was measured by the extrastimulus technique in 16 patients with tachycardia-dependent bundle branch block and 10 patients with functional bundle branch block, both after basic trains of 8 atrial-paced impulses at different cycle lengths and during a 10-min period of continuous overdrive pacing.Results. The baseline refractory period in the bundle branches of patients with functional bundle branch block measured 430 ±32 ms (mean ± SD) and shortened to 368 ± 30 ms at the shortest cycle length. The maximal effect was reached within the 1st min of overdrive pacing. The baseline refractory period of the bundle branches was significantly longer in patients with tachycardia-dependent bundle branch block (611 ± 184 ms) and demonstrated a cumulative overdrive prolongation in 15 (83%) of 18 studies with typical manifestations of fatigue. In two other studies, this occurred only after ajmaline administration.Conclusions. A rate- and time-dependent prolongation of refractoriness frequently occurs in diseased human bundle branches. When absent, this response may be induced under the effects of sodium channel blockers. This would suggest that an abnormality in the recovery from inactivavion of the sodium channel might underlie the early stages of bundle branch disease.

Mechanism of tachycardia-dependent bundle branch block

intervals AzA2 and A2A3 are considerably shorter than 3 and 2 times the pure ectopic cycle length, respectively. Such findings are similar to those in patients with ventricular parasystole. Thus, such findings may be explained in the same manner as in ventricular parasystole. The sinus irapulses P~, P3 and P5 fall after the absolute refractory period of the pathway, and they reach and discharge the parasystolic focus before the occurrence of the next parasystolic impulse. As a result, the interectopic intervals AzA~ and A 2A ~ become shorter than 3 and 2 times the pure parasystolic cycle length, respectively. A nonparasystolic P wave, P7, in the lower part of Figure 1 occurs comparatively early in the parasystolic cycle. The parasystolic cycle that contains this P wave, (A~A4) is the same length as the pure parasystolic cycle that contains no intervening P wave. This indicates that the impulse P7 falls in the absolute refractory period of the pathway, and that the parasystoIic focus is protected from this impulse as shown in the diagram below the strip. Figure 2 also shows that when a nonparasystolic P wave occurs comparatively early in the parasystolic cycle, the parasystolic cycle that contains this P wave (first 3 strips) is almost the same length as the pure parasystolic cycle (bottom strip).

Experimental model for study of Mobitz type II and paroxysmal atrioventricular block

In 26 anesthetized dogs ligation of the anterior septal artery in conjunction with rapid atrial pacing resulted in a relatively high frequency (75 percent) of Mobitz type II block and paroxysmal atrioventricular (A-V) block (50 percent). Electrode catheter recordings from the His bundle and bundle branches as well as plunge wire recordings from the His bundle allowed a localization of block within the ischemic HisPurkinje system within 1 to 4 hours after ligation. Intra-His bundle blocks, manifested as first, second or third degree A-V block, alone or in combination, were found in 18 animals (75 percent). Right bundle branch block was found in 15 and left bundle branch block in 8. Bradycardia- and tachycardia-dependent bundle branch block was a common observation. The use of this preparation has provided insights into the nature of Mobitz type II and paroxysmal A-V block as well as other phenomena usually reported only in clinical settings.

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.