Alternating Wenckebach periods with acute myocardial infarction. Report of two cases.

This report describes two patients with the spontaneous occurrence of alternating Wenckebach periods during the course of acute myocardial infarction. Both patients demonstrated alternating Wenckebach periods which terminated in a sequence of two blocked P waves. In one patient, His bundle electrocardiographic study documented the site of block to be proximal to the His bundle. Alternating Wenckebach periods with the block proximal to the His bundle may be compatible with a benign prognosis.     

Alternating Wenckebach periods occurring in the atria, His-Purkinje system, ventricles and kent bundle

Alternating Wenckebach periods were defined as episodes of 2:1 block during which there was a gradual prolongation of the transmission intervals preceding the appearance of 3:1 or 4:1 block. Alternating Wenckebach periods occurring within the His-Purkinje system in symptomatic patients with right bundle branch block could have resulted from involvement of the His bundle only, the left bundle branch only or both structures simultaneously. Alternating Wenckebach patterns presumably occurring in the reentry pathway of ventricular extrasystoles and in the tissues surrounding an ectopic atrial focus or bipolar pacing electrodes were manifested in the coupling intervals of the premature beats; in the P-P intervals of atrial tachycardia with atrioventricular (A-V) block due to digitalis; and in the stimulus (St)-A intervals following electrical stimuli delivered to the atria at fast rates. Alternating Wenckebach periods of St-H and St-delta wave intervals in patients with the Wolff-Parkinson-White syndrome resulted from involvement of the Kent bundle itself, or of the atria as a proximal level common to distal longitudinally dissociated structures (Kent bundle and A-V node).

It is concluded that contrary to what is commonly believed alternating Wenckebach periods may be a tachycardia-dependent phenomenon occurring above, below or outside the A-V node and explaining a variety of spontaneous or electrically induced arrhythmias whose significance depends on the clinical setting in which they occur.     

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.     

Atrioventricular alternating Wenckebach periodicity: conduction patterns in multilevel block

Atrioventricular (A-V) conduction patterns were analyzed in three patients with atrial pacing-induced alternating Wenckebach periodicity. These cases were unique because in each (1) separate levels of block responsible for the conduction disturbance were located above and below the His bundle recording site, and (2) there were several departures from the simple alternating Wenckebach pattern. Apparent supernormal conduction, temporary 1:1 conduction and a specific form of gap in A-V conduction resulted from the interplay of many factors including a simple mathematic relation of the blocking ratio at the two levels, the characteristics of the Wenckebach cycles, and the cycle length-dependent features of refractory periods at the different sites. The findings indicate that (1) delay in proximal impulse transmission is usually the critical factor in overcoming prolonged distal refractoriness and producing variable conduction patterns during the course of alternating Wenckebach periodicity; (2) many irregularities in alternating Wenckebach periodicity can be explained by known electrophysiologic mechanisms; and (3) simple mathematic equations alone are too rigid to reflect properly the dynamic process underlying this conduction disturbance.     

Effects of proximal intra-atrial Wenckebach on distal atrioventricular nodal, and His-Purkinje, block with special reference to the theory of alternating Wenckebach periods

Intra-atrial Wenckebach patterns of stimulus-to-response intervals coexisting with distal, A-V nodal, and His-Purkinje, blocks occurred in eight patients during high right atrial stimulation at rapid rates. In two patients with 2:1 St-H block and in two patients with 4:1 St-V block, an increase in the degree of block occurred when the proximal intra-atrial Wenckebach cycle was completed with the stimulus which otherwise would have been propagated to the distal levels. However, the degree of block did not increase when the intra-atrial Wenckebach terminated in distally blocked stimuli. In one patient progression of 4:1 into 5:1 St-V block was due to the association of intra-atrial Wenckebach with alternating 2:1 block at the A-V nodal, and His-Purkinje, levels. Contrasting with most reports dealing with the mechanisms of alternating Wenckebach in a single structure, this study permitted the determination of the boundaries between proximal and more distal levels. It also showed that alternating Wenckebach cycles (of St-H intervals) ending with two consecutively blocked stimuli could result from the association of proximal intra-atrial Wenckebach with distal, A-V nodal Wenckebach, or abortive AW, cycles. The electrophysiology of documented two, or three, level block in different structures has validated previously made assumptions regarding multilevel block in a single structure.     

Concealed intraventricular conduction in the His bundle electrogram.

Multiple areas of concealed intraventricular conduction are deduced on the basis of aftereffects observed in His bundle recordings. Electrocardiograms and His bundle recordings are presented from two patients with unstable bilateral bundle branch block, the instability of which depended on the interval at which ventricular depolarization was initiated by sinus or paced impulses. This circumstance allows postulation of 1) concealed transseptal retrograde penetration of the left bundle branch system; 2) concealed transseptal retrograde penetration of the right bundle branch system; 3) alternate beat Wenckebach phenomenon with two areas of block in the bundle branch system with concealed penetration of the proximal area; 4) concealed re-entry in the right bundle branch system during an H-V Wenckebach cycle with resetting of the sequence of 2:1 H-V block and return of the re-entry wave to the A-V node causing subsequent A-H block; 5) proximal 2:1 block and distal Wenckebach block producing only two consecutively blocked beats; and 6) infrahisian Wenckebach block with changes both in A-V conduction and QRS contour.     

Wenckebach periods associated with high grade second degree (2 : 1 and 3 : 1) A-V block.

An electrocardiogram (ECG) of bilateral bundle branch block (BBBB) which may be attributable to a mixture of 2 : 1 and 3 : 1 atrioventricular (A-V) block is described. The irregularity of QRS complexes with left bundle branch block (LBBB) pattern during 2 : 1 A-V block may be ascribable to "Wenckebach periods", which might be due either to A-V nodal or His bundle or bundle branch delay. However, it was impossible to distinguish between them precisely because appropriate His bundle studies were not performed during the active arrhythmic phase. Although the exact mechanism involved were not established with certainty, different rates of recovery in conduction in the bundle branches in association with a marked prolongation of the refractoriness would seem to be the unique feature of this complex arrhythmia. An ECG tracing of BBBB indicating high grade second degree (2 : 1 and 3 : 1) A-V block, in which "spontaneous" occurrence of "Wenckebach periods" with 2 consecutive blocked P waves can be observed during 2 : 1 A-V block, has never been reported previously as far as can be ascertained from published records.     

Atrial tachycardia, 2:1 alternate Wenckebach periodicity, and atrial standstill

A case of atrial tachycardia, 2:1 alternate Wenckebach periodicity and atrial standstill is reported in an 80-year-old woman who complained of exertional dyspnea and occasional syncope for two years. Two blocked P' waves appeared after each Wenckebach period suggesting type B alternating Wenckebach phenomenon (Mobitz type II 2:1 A-V block distal, and Wenckebach conduction proximal).     

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.     

His bundle electrocardiography in digitalis-induced "atrioventricular junctional" Wenckebach periods with irregular H-H intervals.

His bundle electrograms were recorded during catheter insertion for prophylactic demand pacing in two patients with accelerated or nonaccelerated "atrioventricular (A-V) junctional" rhythms associated with A-V junctional Wenckebach periods. This appears to be the first published report of so-called A-V junctional Wenckebach periods in which the characteristic irregularities of the H-H intervals were recorded. Patient 1 had an additional area of "complete" anterograde A-V nodal (A-H) block. In Patient 2 the rate of impulse formation was consistent with nonparoxysmal A-V junctional tachycardia. The His bundle recordings were obtained in patients with digitalis toxicity and should be interpreted in the context. The integration of clinical and intracardiac findings with extrapolations from microelectrode and pharmacolic studies and with deductions from the clinical electrocardiograms suggests that the conduction disturbances probably occurred within the A-V node itself (in its AN region). This hypothesis implies that automaticity also originated in the A-V node because the site of impulse formation must have been proximal to the site of the Wenckebach periods. However, conclusive proof of of these postulates will require further studies with refined techniques.     

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.     

Electrophysiologic observations in a patient with bradycardia-dependent atrioventricular block

In a patient with atrioventricular (A-V) block distal to the His bundle (H), 1:1 A-V conduction with right bundle branch block and an H-V interval of 70 msec was established with atrial pacing at rates of 120 to 150/min, suggesting that the A-V block was bradycardia-dependent. Advanced second degree A-V block distal to the H deflection occurred with atrial pacing at 160/min after completion of A-V nodal Wenckebach periodicity proximal to the H deflection because of the long H-H encompassing the blocked P wave. Atrial extrastimulus testing coupled with sinus rhythm (with A-V block) demonstrated that critical H₁-H₂ intervals of less than 545 msec allowed conduction to the ventricles. The H₂-V₂ interval shortened progressively from 290 to 70 msec with shortening of these critical H₁-H₂ intervals. Atrial extrastimulus testing coupled with an atrial driven cycle length of 500 msec (with intact A-V conduction) revealed block of the H₂ deflection with an H₁-H₂ interval longer than 540 msec.In conclusion, at critical diastolic intervals, impulses were blocked, creating a state of decreased responsiveness. If a cycle length of subsequent impulses was shorter than the critical diastolic blocking interval, membrane responsiveness gradually improved and conduction resumed. If a cycle length of subsequent impulses was longer than the critical blocking diastolic interval, A-V block was sustained. Blocked impulses continually penetrated to the site of block and reset the state of membrane responsiveness.     

Electrocardiographic patterns during Holter monitoring in patients with first and second degree A-V block due to 'dual A-V nodal pathways'

The electrocardiographic patterns, observed during 24-h Holter monitoring, of 10 patients (mean age 35 +/- 22 years) with first and second degree A-V block due to dual A-V nodal pathways are reported. Recordings were selected according to the presence of: sudden and persistent prolongation of the PR interval: sudden normalization of the PR interval: 'atypical' Wenckebach sequences showing sudden and pronounced prolongation of any PR interval prior to the blocked P wave. Besides the already recognized pattern, new aspects were identified: (1) Wenckebach sequences in the slow and fast pathways characterized by a progressive increase in the PR interval until a blocked P wave occurred during long and short PR interval periods, respectively; (2) Wenckebach periods first in the slow and then in the fast pathway; (3) 2:1 A-V block with a normal PR interval in the conducted beat after a Wenckebach sequence in the slow pathway; (4) Wenckebach in the fast pathway and, subsequently, in the slow one characterized by a slight prolongation of the PR interval for some beats followed by a sudden and pronounced increase in the PR interval of one beat and a subsequent progressive slight PR prolongation until a blocked P wave occurred; (5) Wenckebach sequence in the fast pathway with subsequent conduction over the slow pathway without a blocked P wave; (6) blocked P waves during both long and short PR interval periods with slight prolongation of the preceding PR interval. The electrophysiological mechanisms involved in these electrocardiographic patterns together with the nature (anatomical or functional) of the intranodal pathways and the clinical significance of this type of block are discussed.     

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.     

Electrophysiologic studies in Mobitz type II second degree heart block

The electrophysiologic basis for Mobitz type II second degree heart block was studied in a patient with documented episodes of complete heart block and Stokes-Adams seizures. Recording of His bundle electrograms demonstrated that all atrial impulses were conducted through the atrioventricular (A-V) node to the bundle of His. Nonconducted P waves were blocked distal to the bundle of His. The frequency of blocked beats increased when the rate was accelerated by atrial pacing. Administration of atropine caused more frequent blocked beats, reaffirming the concept that the block occurred beyond the node. It is concluded that Mobitz type II second degree heart block is a manifestation of bilateral bundle branch block. Testing with atropine in this case was useful in distinguishing block in the bundle branches from that in the A-V node.     

Influence of pacemaker-induced tachycardia with A-V block on left ventricular blood velocity in man.

Phasic instantaneous left ventricular blood velocity was measured by radiotelemetry in 28 subjects with a Doppler ultrasonic flowmeter catheter during atrial pacing and induced A-V block Type I Wenckebach A-V block with conduction ratios of 9:8 or lower generally produced a stepwise reduction of peak left ventricular blood velocity in relation to shortened R-R intervals. Longer Wenckebach periods resulted in little or no blood velocity alteration during 1:1 A-V conduction. Those beats following a blocked atrial depolarization were associated with augmented blood velocities. In three subjects, bigeminal periods of 3:2 A-V block resulted in larger left ventricular blood velocities when compared with 2:1 A-V block, despite identical R-R intervals following the blocked P wave. This latter phenomenon was attributed to diastolic augmentation of left ventricular contraction following the second and hemodynamically ineffective beat during 3:2 A-V block. Three patients manifested true blood velocity alternation during second-degree A-V block and changing R-R intervals. The variations in peak left ventricular blood velocity observed during atrial pacing and A-V block are related to changing inotropic state and cycle length dependent alterations of left ventricular diastolic filling.     

Patterns of atrioventricular conduction in children.

In this study, intracardiac electrograms were performed in 20 children--ranging in age from eight months to 18 years and without evidence of conduction disturbances on the scalar electrocardiogram--to determine the normal conduction patterns, response to atrial pacing, and values of refractory periods. Atrial pacing--18 cases--induced a prolongation al AH on increasing heart rates in all; 11 developed Wenckebach block proximal to the bundle of His at the mean pacing rate of 224 per minute +/- 45 (1 S.D.). Refractory periods were shorter than in adults. Study of the pattern of A-V conduction revealed three types of response: (1) the atrium was the limiting structure in 11 cases; (2) the delay occurred in the A-V node only in four cases; and (3) the delay occurred both in the A-V node and His-Purkinje system. This response was observed in one case only.     

Significance of A-H interval in patients with chronic bundle branch block. Clinical, electrophysiologic and follow-up observations.

His bundle electrograms were recorded in 308 adults with chronic bundle branch block. The A-H interval was normal in 249 patients and prolonged in 59. Comparison of patients with normal and prolonged A-H intervals revealed a greater incidence of demonstrable organic heart disease in the latter (P less than 0.01). Dyspnea, cardiomegaly and congestive heart failure were more frequent in patients with A-H prolongation. These patients also had longer P-R intervals and atrioventricular (A-V) nodal effective refractory periods, lower paced rates producing second degree A-V block proximal to the His bundle and a greater frequency of H-V prolongation. All patients were prospectively followed up in a conduction disease clinic with mean follow-up periods (+/- standard error of the mean) of 523 +/- 23 and 588 +/- 47 days in the patients with normal and prolonged A-H intervals, respectively. Seven (3 percent) of the patients with a normal A-H interval had A-V block with probable or definite site of block proximal to the His bundle in three and distal to the His bundle in four. In five of the six patients with a prolonged A-H interval who experienced A-V block (10 percent), the probable or definite site of block was proximal to the His bundle. Mortality (both sudden and nonsudden) was not significantly different in the patients with normal and prolonged A-H intervals. In summary, A-H prolongation was associated with increased incidence of organic heart disease and myocardial dysfunction. The risk of development of A-V nodal block was greater in patients with a prolonged A-H interval but appeared to be of minimal clinical significance.     

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.