Coexisting intra- and subnodal block: an unusual abnormality of atrioventricular conduction

The presence of A-V block occurring at two levels of the conducting system was demonstrated in an asymptomatic patient by means of the His bundle recordings. During sinus rhythm, first degree A-V block with complete left bundle branch block was noted, suggesting the presence of bilateral bundle branch block. His bundle recordings demonstrated the coexistence of intranodal (Wenckebach periods, Mobitz Type I) and subnodal (Mobitz Type II) block. The evidence of block below the proximal His bundle offered confirmatory evidence of bilateral bundle branch block. In spite of the abnormal antegrade conduction, there was 1:1 V-A conduction during right ventricular pacing at 110 per minute. With more rapid (130 per minute) ventricular pacing, retrograde Wenckebach periods were observed, suggesting that there was, in addition, possible impairment in retrograde conduction. This report serves to demonstrate (1) the limitations of the body surface ECG in the assessment of A-V conduction and (2) that His bundle electrograms make it possible to detect the presence of coincidental lesions at two levels of the A-V conducting system.     

Termination of circus movement tachycardia utilizing an accessory atrioventricular pathway by retrograde concealed penetration of the atrioventricular node through the bundle branch system: A mechanism of tachycardia termination in Wolff-Parkinson-White syndrome

A 30 year old woman with Wolff-Parkinson-White syndrome underwent electrophysiologic study for investigation of circus movement tachycardia utilizing the accessory pathway for retrograde conduction. The accessory pathway was located on the right side. Episodes of circus movement tachycardia with left and right bundle branch block were induced. Some episodes of circus movement tachycardia with left bundle branch block terminated spontaneously. Two episodes of spontaneous termination at the level of the atrioventricular (A-V) node were preceded by prolongation of the H-V interval causing delay in atrial activation. This delayed atrial cycle was then followed paradoxically by spontaneous termination of the tachycardia in the A-V node. A similar phenomenon could be demonstrated reproducibly with single echo beats induced by coronary sinus extrastimuli. It appears that retrograde concealed penetration of the A-V node through the bundle branch system during anterograde left bundle branch block is the most likely mechanism for this phenomenon.     

Atrial response during ventricular fibrillation

Electrical activity of the bundle of His and atria were recorded during sinus rhythm and electrically induced ventricular fibrillation in 23 dogs. Multiple bipolar atrial electrograms obtained from several sites within the right and left atria permitted the determination of the frequency, regularity, and sequence of atrial activation (i.e., sinus or retrograde) during ventricular fibrillation. Prior to the induction of ventricular fibrillation, the capacity to retrogradely conduct across the A-V node was tested in each animal by pacing the right ventricle at various cycle lengths. Fourteen animals demonstrated consistent 1:1 retrograde conduction at various paced cycle lengths (Group A); in four animals (Group B) retrograde conduction was intermittent and in three animals (Group C) no retrograde conduction was observed at any paced cycle length. Ventriculo-atrial conduction was also absent in two animals (Group D) with antegrade A-V block within the His-Purkinje system.The most common conduction pattern noted at the onset of ventricular fibrillation was that of rapid, irregular, retrograde activation of both the bundle of His and atria. However, the frequency of retrograde activation of the atria was less than that of the bundle of His indicating that the A-V node was a site of retrograde concealment of impulses. This conduction pattern was noted in all animals of Groups A and B. In all animals of Groups C and D, the atria continued to be activated in a sinus sequence during ventricular fibrillation. In Group C animals, the A-V node was the site of both antegrade and retrograde concealment. In the two animals with A-V block (Group D), the site of retrograde concealment was distal to the site of block.In six studies, retrograde A-V nodal Wenckebach cycles with and without re-entry were observed for varying periods of time.Less often, the irregular atrial responses during ventricular fibrillation were accounted for by short periods of sinus capture interspersed with periods of retrograde capture.During ventricular fibrillation, retrograde conduction across the A-V node could be abolished by vagal stimulation.The results of this study indicate that retrograde concealed conduction within the A-V node is the major determinant of an irregular atrial response during ventricular fibrillation just as antegrade concealed conduction is the major determinant of an irregular ventricular response during atrial fibrillation.     

Conduction system in a patient with Prinzmetal's angina and transient atrioventricular block.

His bundle recordings obtained during and between attacks of Prinzmetal's variant angina and transient atrioventricular (A-V) block were followed by a comprehensive serial section study of the conduction system in a 33 year old woman. Recordings between attacks showed normal A-H and H-V intervals. During an attack there was block proximal to the His bundle recording site. Pathologic studies revealed severe narrowing of the right coronary artery. Arteriolosclerosis of the heart was diffuse. Insignificant changes were found in the approaches to the A-V node and the A-V node itself. Major changes found in the left bundle branch had no counterpart in the electrocardiogram; the discordance in these findings is discussed.     

Re-entry due to manifest and concealed. His bundle ectopic systoles. Report of a case.

Concealed (C) His bundle ectopic systoles (H') have been shown in man to give rise to first and second degree atrioventricular (A-V) block and to simulate nonconducted atrial premature beats (P'). This report outlines a hitherto undescribed electrophysiologic consequence of H' in a 69-year-old man with arteriosclerotic heart disease and a Wenckebach type second degree A-V block in the His-Purkinje system. During a His bundle study, H' were shown to conduct either to the atria and ventricles with varying relationships to P' and QRS, or to conduct only to the atria, simulating nonconducted P' or atrial fusion beats. Both types of H' could initiate a re-entrant arrhythmia during retrograde conduction. Of particular interest are late coupled H' that failed to conduct to the ventricles and also failed to activate the atria because of prior capture by the sinus impulse (CH'). These CH' could also initiate re-entry by conducting retrogradely to engage the subatrial re-entry circuit. Evidence is presented to suggest re-entry occurs by way of a retrograde concealed accessory pathway and antegrade conduction in the atrioventricular node.     

Pseudo A-V block associated with A-H and H-V conduction defects

His bundle electrograms were recorded in a patient with tertiary syphilis whose ECG's showed right bundle branch block, junctional premature systoles, and episodes suggesting both Mobitz Type I and II second degree A-V block. Junctional premature depolarizations were found to cause: (1) ventricular systole, (2) retrograde atrial depolarizations with atrial fusion, and (3) nonconducted P waves of normal contour (pseudo A-V block). Nonconducted nonpremature P waves were also noted to occur secondary to both A-H and H-V forms of second degree A-V block in the absence of junctional premature activity.The presence of an H-V conduction defect may cause antegrade block of junctional premature depolarizations and enhance their expression as pseudo A-V block. This term should, therefore, not be meant to imply A-H and H-V conduction.     

Electrophysiologic and pathologic correlations in two cases of chronic second degree atrioventricular block with left bundle branch block.

This study concerns two cases of chronic 2 degrees atrioventricular (A-V) block with left bundle branch block (LBBB). Pathological studies included serial section of the conduction systems. Case 1 had type I 2 degrees block with LBBB. Electrophysiological studies revealed type I 2 degrees block proximal to the His bundle recording site and a prolonged H-V interval (60 msec). Pathologically there was a moderate to marked fibrosis of the approaches to the A-V node and of the A-V node, marked fibrosis of the left bundle branch, and moderate involvement of the right bundle branch. The changes proximal to the His bundle were more marked than the changes distal to this bundle. Case 2 had type II and 2:1 2 degrees A-V block with LBBB. Electrophysiologically the site of block was distal to the His bundle recording site, and there was a prolonged A-V node and severe involvement of both bundle branches. The changes distal to the His bundle were more severe than the changes proximal to the His bundle. This study reveals that the electrophysiologic data more closely approximated the pathologic findings than did surface electrocardiographic data alone. It also emphasizes that there may be multiple sites of disease in chronic 2 degrees block with bundle branch block.     

His bundle electrocardiography in manifest and concealed right bundle branch extrasystoles.

His bundle electrocardiography was helpful in the diagnosis of impulse formation in the right bundle branch. Ten patients with narrow QRS complexes had ectopic beats with an "incomplete" left bundle branch pattern and almost simultaneous activation of His bundle and ventricles. Both QRS morphology and H- - V intervals depended on the more proximal or distal location of the ectopic focus. In four patients with "complete" right bundle branch block the morphology of ectopic ventricular complexes and H- - V intervals also depeneded on the presence or absence of retrograde block and differential degrees of forward and/or retrograde conduction delays. Nine patients with "complete" right bundle branch block and four with "complete" left bundle branch block had premature beats which could have originated in the proximal right bundle branch, proximal left bundle branch, or distal His bundle. In one patient with "complete" left bundle branch block, "concealed" His bundle depolarizations (probably originating in an ectopic focus located in the right bundle branch) produced pseudo Type II (Mobitz) A-V block. Although lidocaine appeared to have been more effective in patients with bundle branch block than in those with narrow QRS complexes, further studies are necessary to corroborate this impression.     

Alternative mechanisms of apparent supernormal atrioventricular conduction

Alternative mechanisms were found to explain several different electrocardiographic examples of apparent supernormal atrioventricular (A-V) conduction in man using programmed premature atrial and ventricular stimulation and His bundle recordings. Sudden shortening of the P-R interval during A-V nodal Wenckebach phenomenon was due to manifest or concealed reentry within the A-V node. Gap phenomena in which late atrial premature depolarizations blocked while earlier atrial premature depolarizations conducted were shown to result from delay of earlier atrial premature depolarizations in the A-V node (type I gap) or in the His-Purkinje system (type II gap). Mechanisms analogous to the latter were found in cases of apparent supernormality of intraventricular conduction: Late atrial premature depolarizations resulted in aberration whereas earlier atrial premature depolarizations conducted normally because of delay within the A-V node or His-Purkinje system. Unexpected normalization of a bundle branch block pattern also resulted from Wenckebach phenomenon in the bundle branches. Atypical Wenckebach phenomenon with the first beat of the period demonstrated that aberration was due to phase 4 depolarization. Preexcitation of the ventricle before the delivery of a previously blocked atrial premature depolarization allowed conduction through the area of block (A-V node) because of earlier depolarization of the latter with earlier recovery. In the His-Purkinje system, 2:1 A-V block was converted to 1:1 conduction when a premature ventricular depolarization shortened the refractoriness of the His-Purkinje system.     

Observations during clinical 2:1 and 3:1 A-V block below the A-V node. Evidence of partial penetration of atrial impulses into the His bundle

A clinical His bundle recording during 2:1 A-V block below the A-V node displayed RBBB, a prolonged H-V interval, and alternating amplitude and duration of the His potentials. The reduced amplitude of the non-conducted His potential suggests a lesser depth of penetration into the His tissue with subsequent block. The reduced His potential amplitude may be due to decremental conduction within the His bundle and/or prolonged refractoriness of the His tissue following atrioventricular conduction of the preceding atrial impulse.During 3:1 A-V block progressively deeper penetration of the atrial impulses into the His-Purkinje system occurred. Progressive penetration into the more proximal His-Purkinje system may have permitted recovery of a more distal area of refractoriness with subsequent atrioventricular conduction. This mechanisms appears similar to one of the mechanisms of 3:1 A-V block demonstrated experimentally, except that in this clinical record the major site of impaired conduction and progressive penetration is within the His-Purkinje system rather than within the A-V node.     

Effect of intravenous amiodarone in patients with intraventricular conduction disorders

Using His bundle recordings and stimulation techniques, theelectrical effects of amiodarone (5 mg/kg intravenously) wereassessed in 12 patients aged 34–80 years (mean 65) exhibitingin sinus rhythm, intraventricular conduction disturbances. Bundlebranch block was present in 10 patients: left bundle branchblock in three patients, right bundle branch block in three,bilateral bundle branch block in four. All the patients hada long H-V interval (65–80 ms; mean 71). As has been previouslyreported, amiodarone slowed the sinus rate, prolonged the QTinterval, increased the atrial effective refractory period anddepressed A-V nodal conduction. Despite the presence of advancedconduction disturbances within the His-Purkinje system, amiodaronedid not alter the H-V interval in 11 patients and increasedit in one by only 5 ms. Thus, clinically, the use of amiodaronein patients with bundle branch block should be safe.     

Anterograde and retrograde bradycardiac block in the His-Purkinje system. Finding in a patient with acute myocardial infarction

A patient with an acute inferior myocardial infarction developed a complete atrioventricular block and intermitent periods of atrioventricular conduction with QRS complexes showing right bundle branch block associated with left anterior hemiblock. Recordings of the His bundle electrogram showed that the atrioventricular block was infrahisian and that in periods of resumed atrioventricular conduction, the His-ventricle (H-V) interval was long. Ventricular escape beats showed concealed conduction to the atrioventricular node. Anterograde atrioventricular conduction was always resumed through the left posterior division when the preceding division when the preceding intervals between ventricular escape beats and the atrium (V-A intervals) were shorter than 580 msec. The same phenomenon occurred with right ventricular pacing. A retrograde His potential could be observed. Retrograde conduction of ventricular escape beats and ventricular paced beats was blocked if the H-V interval and the interval between the His bundle and the ventricular paced beat (H-V interval) were long (more than 600 msec and 550 msec, respectively). The existence of an intermittent anterograde and retrograde bradycardiac infrahisian block was inferred from the previously mentioned data; a fixed retrograde atrial nodal block was also present.     

Atrioventricular block after reciprocating atrioventricular junctional tachycardia.

Short runs of symptomatic atrioventricular (A-V) block occurred after spontaneous cessation of reciprocating A-V junctional tachycardia in a patient with right bundle branch block, normal H-V interval and sinus nodal dysfunction. These episodes were characterized by long (more than 1 sec) P-P intervals during which the A deflections were not followed by His bundle electrograms. Three possible explanations are: (1) a posttachycardia-induced period of abnormally prolonged A-V nodal refractoriness; (2) pseudo-A-V block produced by concealed A-V junctional tachycardia, or (3) bradycardia-dependent (phase 4) A-V block at the "upper" His bundle, above the site from which the H deflection was recorded.     

Alternating Wenckebach periodicity: A common electrophysiologic response.

Alternating Wenckebach periods are defined as episodes of 2:1 atrioventricular (A-V) block in which conducted P-R intervals progressively prolong, terminating in two or three blocked P waves. In this study, His bundle recordings were obtained in 13 patients with pacing-induced alternating Wenckebach periods. Three patterns were noted: Pattern 1 (one patient with a narrow QRS complex) was characterized by 2:1 block distal to the H deflection (block in the His bundle) and Wenckebach periods proximal to the H deflection, terminating with two blocked P waves. Pattern 2 (four patients) was characterized by alternating Wenckebach periods proximal to the His bundle, terminating with three blocked P waves. Pattern 3 (eight patients) was characterized by alternating Wenckebach periods proximal to the His bundle, terminating with two blocked P waves. Alternating Wenckebach periods are best explained by postulating two levels of block. When alternating Wenckebach periods are terminated by three blocked P waves (pattern 2), the condition may be explained by postulating 2:1 block (proximal level) and type I block (distal level). When alternating Wenckebach periods are terminated by two blocked P waves (patterns 1 and 3), the condition may be explained by postulating type I block (proximal level) and 2:1 block (distal level). Pattern 1 reflects block at two levels, the A-V node and His bundle. Patterns 2 and 3 most likely reflect horizontal dissociation within the A-V node.     

Bundle branch block on alternate beats: by what mechanism?

In a patient with right bundle branch block occurring on alternate beats during regular sinus rhythm, the conduction disturbance disappeared during hyperventilation induced increase in heart rate, and reappeared with slight slowing of the sinus rate due to carotid sinus massage. The following mechanisms are potentially involved in the electrogenesis of bundle branch block alternans with regular RR intervals: a) phase-3 2:1 bidirectional block; b) phase-3 antegrade block with retrograde concealed activation of the involved bundle branch and subsequent "supernormal" conduction; and c) phase-4 antegrade block with transseptal retrograde concealed invasion of the affected bundle branch by impulses traversing the unimpaired bundle branch. Analysis of the tracing excluded both mechanisms a and b and favored bradycardia-dependent right bundle branch block as a key to explain the alternate pattern of intraventricular conduction.     

Wenckebach periods with repetitive block: evaluation with His bundle recording

Two patients are reported in whom repetitive block of two consecutive P waves occurred during Wenckebach beating induced by atrial pacing. His bundle recordings revealed block proximal to H in the first case, suggesting inhomogeneous conduction in the A-V node. In the second case, long cycle lengths were produced in the His-Purkinje system due to A-V nodal Wenckebach periods. The long cycles prolonged refractory periods in the His Purkinje system so that subsequent beats (short cycles) were blocked distal to H.The repetitive block of consecutive multiple atrial impulses could result in unexpected degrees of ventricular asystole during usually benign Type I second-degree A-V block.     

Exposure of concealed right bundle branch block in Wolff-Parkinson-White type B by pacing from the vicinity of the A-V node.

In two infants with Wolff-Parkinson-White type B, right bundle branch block was concealed during sinus rhythm and pacing from close to the atrial entrance of the right-sided accessory pathway. However, pacing from the vicinity of the A-V node, the A-V node itself, and the His bundle exposed the right bundle branch block by producing exclusive ventricular activation through the normal, A-V nodal His-Purkinje pathway. In addition, pacing from close to the A-V node also resulted in fusion beats characterized by absence of delta waves with (pseudo) normal QRS complexes and short H-V intervals. False patterns of tachycardia-dependent and bradycardia-dependent block in the accessory pathway also occurred. These dynamic phenomena were attributed to the (peri-A-V nodal) pacing-related, relatively early arrival of excitation at the ventricles through the normal pathways coexisting with delayed arrival of excitation via the accessory pathway. The latter in turn was due to the longer intra-atrial conduction time from paced (peri-A-V nodal) site to atrial entrance of the accessory pathway.     

Alternating right and left bundle branch block aberration during atrial tachycardia

In a patient with atrial tachycardia with a rate of 200 per minute, the A-V conduction ratio was at times 2:1, but often it was 4:3 or 3:2 with progressive P-R interval prolongation (Wenckebach mechanism, an expression of presumable A-V nodal block). In each episode of 4:3 conduction, the first QRS complex was narrow, and the 2 ensuing beats were wide due to aberrant conduction. Aberration did not occur with a constant configuration, but in consecutive episodes of 4:3 conduction ratio there was a regular alternation of left bundle branch block and right bundle branch block. The pattern was explained by concealed retrograde conduction into the anterogradely blocked bundle branch. This caused 2 distinct effects: (1) shifting “to the right” of the refractory period of the affected bundle branch, resulting in maintenance of aberration with the same configuration, if consecutive atrial impulses were conducted to the ventricles, and (2) shortening of the effective cycle of the affected bundle branch, resulting in aberration due to block of the controlateral bundle branch, whenever a pause occasioned by a nonconducted atrial impulse was followed by restoration of 1:1 conduction for 2 or more consecutive beats.     

A demonstration of differential refractoriness within a single fascicle of the human ventricular specialized conduction system

In 15 patients with left bundle branch block (LBBB), atrial (A), His bundle (H), and ventricular (V) electrograms were recorded. Successively more premature atrial depolarizations were introduced via a catheter in the right atrium. In eight patients, the ventricular specialized conducting system (VSCS) was the most refractory portion of the entire atrioventricular conducting system (AVCS) and A-V conduction, which had been occurring via the right bundle branch (RBB), failed below the His bundle as the effective refractory period (ERP) of the VSCS was reached. In two of these eight patients, after the ERP of the VSCS was exceeded, further shortening of the H₁-H₂ interval (by 40 to 50 msec.) resulted in an unexpected resumption of A-V conduction, but with markedly prolonged H-V intervals (160 to 230 msec.). This demonstrates that differential refractoriness exists within the RBB of these patients. A zone of maximal refractoriness was initially encountered within the RBB when the premature impulse first blocked below the His bundle. In relative terms, this zone was distal to a more proximal area of the RBB where, with further shortening of the H₁-H₂ interval, sufficient conduction delay occurred to permit recovery of excitability distally and the resumption of A-V conduction.     

Coexistent Wenckebach phenomenon in the distal branches of the specialized conduction system

A patient in whom Wenckebach phenomenon was observed to coexist in the three distal branches of the specialized ventricular conduction system, with an intermittent trifascicular block producing a second degree A-V block, is described. Surface electrocardiogram demonstrated the presence of this phenomenon in the right bundle branch (RBB) and the anterior division of the left bundle branch (LBB). Evidence of the presence of Wenckebach phenomenon in the remaining fascicle was provided by His bundle recording.