Electrophysiological and clinical observations in patients with alternating bundle branch block.

Electrophysiological studies (His bundle recordings and atrial stimulation) were performed in nine patients who manifested periods of both right and left bundle branch block (RBBB and LBBB). In seven of the patients, alternating bundle branch block appeared to reflect intermittent or chronic bundle branch block superimposed on incomplete (but electrocardiographically complete) block of the contralateral bundle branch. In three of these seven, shift from one bundle branch block pattern to the other was associated with reproducible change in H-V (mean change 30 msec), and could be induced by alteration of cardiac rate with carotid massage, coupled atrial stimulation, and rapid atrial pacing. In one of the seven, RBBB with a P-R of 0.20 seconds preceded chronic LBBB with a P-R of 0.24 seconds, implying that RBBB had been incomplete. In three of the seven, although a definite mechanism of alternation could not be demonstrated, transient contralateral bundle branch block occurred superimposed on chronic ipsilateral bundle branch block, implying that the ipsilateral block was incomplete. Two patients manifested periods of narrow QRS, LBBB, RBBB, and paroxysmal A-V block. Based upon pathological data (one case), this pattern appeared to reflect a lesion involving the distal His bundle and proximal bundle branches. In the total group of patients, clinical course was primarily determined by the severity of heart disease and not by occurrence of A-V block. The conduction defect in the majority of patients was surprisingly benign.     

Effects of stable and changing rates and premature ventricular beats on transient tachycardia-, pseudobradycardia-, and bradycardia-dependent bundle branch block alternans.

New circumstances under which bundle block (BBB) alternans may appear or disappear are described. 1) Tachycardia-dependent as well as bradycardia-dependent BBB alternans may begin after constant BBB is interrupted by a premature ventricular beat. Tachycardia- and bradycardia- dependence may be differentiated by the shape of the first beat after the pause. 2) When BBB alternans disappears during a constant ventricular rate, tachycardia-dependent BBB alternans changes to persistent normal or more normal intraventricular conduction, whereas bradycardia-dependent BBB alternans changes to a persistently greater degree of BBB. 3) BBB alternans appears to be tachycardia- or pseudobradycardia-dependent in relation to the cycle length and antegrade and retrograde refractory periods in the involved bundle branch. 4) BBB alternans may be recognized during persistent irregular ventricular action in atrial fibrillation. Here the recognition of BBB alternans depends upon the sequence of contours as well as upon the cycle lengths.     

Arrhythmias in the coronary-care unit. V. Physiologic bases of paroxysmal bradycardia-dependent bundle branch block.

Bradycardia-dependent bundle branch block can occur during acute cardiac ischemia or infarction. Basic cellular electrophysiology helps in understanding the mechanisms involved. A review of the previous four vignettes of this series will be helpful in studying this vignette.     

Tachycardia- and bradycardia-dependent atrioventricular block: observations regarding the mechanism of block

A case of paroxysmal bradycardia- and tachycardia-dependent atrioventricular (AV) block is described in a patient with right bundle branch block. The His bundle recordings demonstrated the site of the AV block to be distal to the His bundle recording site (probably in the left bundle branch). Whereas AV block distal to the His bundle occurred at an atrial paced cycle length of 700 ms, intact ventriculoatrial (VA) conduction was present up to a ventricular paced cycle length of 400 ms. Resumption of AV conduction was dependent on a critical HH or RH (in case of escapes) interval. These findings suggest that the bradycardia-dependent block is related to a time-dependent decrease in the amplitude of the current intensity of the proximal segment during late diastole. Spontaneous diastolic depolarization during late diastole resulted in impaired anterograde (AV) conduction but facilitated retrograde (VA) conduction. These findings are consistent with experimental "in vitro" observation in the sucrose gap model of AV block.     

Apparent bradycardia-dependent right bundle branch block associated with atrial fibrillation: concealed electrotonic conduction as a possible mechanism

A 79-year-old woman with atrial fibrillation was reported in whom apparent bradycardia-dependent right bundle branch block was suggested. When a conducted supraventricular impulse occurred within a critical period after the preceding conducted impulse, the impulse was blocked in the right bundle branch except when it fell in the supernormal period of the right bundle branch. When the conducted impulse occurred between the critical period and another longer period, it was conducted without bundle branch block. When the impulse occurred beyond that longer period, it was usually blocked in the bundle branch again. However, when the impulse occurred beyond a still longer period, it was conducted without bundle branch block again. These findings suggest that when impulses fell in the right bundle branch shortly after the preceding conducted impulses, they were blocked in both bundle branches; however, it seemed that concealed electrotonic conduction of the blocked impulses affected conduction of the subsequent impulses.     

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.     

Exercise-induced bundle branch block

Exercise-induced bundle branch block (BBB) is poorly understood. An investigation was made of its clinical, electrocardiographic, coronary angiographic, and myocardial scintigraphic characteristics, with follow-up data in 16 patients, aged 59 ±9 (mean ± standard deviation) years, 11 who had left BBB and 5 who had right BBB. Fourteen had a preexisting baseline electrocardiographic abnormality; 11 had either incomplete BBB or nonspecific intraventricular conduction delay. Heart rates at onset of exercise BBB varied from 70 to 166 beats/min and in 9 patients the rates at BBB onset and offset appeared to be related, occurring within 8 beats/min of each other. Coronary artery disease (CAD) was diagnosed in 10 patients, cardiomyopathy in 2, and probable coronary spasm in 2. One patient had ventricular arrhythmias of uncertain origin, and 1 appeared to have no cardiac disease. Three patients had reversible thallium perfusion defects consistent with ischemia concurrent with developing BBB. The 3 patients in whom exercise BBB persisted all had CAD. Over a mean of 28 months of follow-up, only 1 patient had a morbid cardiac event—nonfatal myocardial infarction—and 2 died from noncardiac causes. Thus, exercise BBB primarily occurs in the context of cardiac disease, most commonly CAD, and concurrent ischemia may be demonstrable; the presence of “rate relation” does not militate against CAD.     

His bundle recordings in bradycardia-dependent AV block induced by premature beats.

Symptomatic bradycardia-independent atrioventricular block occurred in a patient with right bundle-branch block, left anterior hemiblock, and prolonged HV interval. The arrhythmia, triggered by a spontaneous or induced premature beats, appeared when the post-extrasystolic PP and HH intervals increased to a critical value. Reinitiation of atrioventricular conduction required the presence of ventricular escapes. Bradycardia-dependent atrioventricular block was related to either an enhanced or slightly rising slope of diastolic depolarization, or to a decrease in membrane responsiveness. The patient also, most probably, had tachycardia-dependent atrioventricular block. Both types of conduction disturbance occurred in the same part of the intraventricular conducting system, either in the low His bundle or left bundle-branch or its posteroinferior division. It is suggested that the electrophysiological study of cases with prolonged HV intervals should include procedures which can expose bradycardia-dependent atrioventricular block.     

Prospective observations in patients with chronic bundle branch block and marked H-V prolongation.

Eighteen of 388 patients with chronic bundle branch block, studied electrophysiologically and followed prospectively, had H-V intervals of 80 msec or greater. Five patients were functional class I, five class II, seven class III, and one class IV. Follow-up ranged from 103 to 1919 days (mean 711 +/- 118). Three patients needed permanent pacing for the following indications: sino-atrial block, sinus bradycardia post-cardiac surgery, and 2 degrees block distal to the His bundle. Six patients died, three suddenly, and three nonsudden. The five initially asymptomatic patients are alive and without pacemakers (mean follow-up 732 +/- 139 days). Although marked H-V prolongation was associated with high morbidity and mortality in this small series, this was only in patients with symptomatic heart disease. Asymptomatic patients (five patients) had a benign clinical course. Prophylactic pacing would probably not modify clinical course in the former group, and is probably not indicated in the latter group. Longer follow-up will be needed for definitive prognostication.