Atrioventricular Wenckebach periodicity in athletes: influence of increased vagal tone on the occurrence of atypical periods

In 37 athletes with atrioventricular (AV) Wenckebach periodicity, the relationship between PP and RR intervals was investigated. In most athletes, when PP intervals gradually lengthened, RR as well as PR intervals usually also gradually lengthened until a blocked P wave occurred, resulting in the occurrence of an atypical Wenckebach period with prolongation of the last RR interval (variant I). In 20 athletes, sudden marked prolongation of a PR interval occasionally occurred, which was usually followed by a blocked P wave (variant II). In five athletes, once sudden marked prolongation of a PR interval occurred, markedly long PR intervals were maintained for some time, and then a PR interval suddenly shortened without a blocked P wave (variant III). It appeared that the above findings were caused by spontaneous variations in vagal tone. It was suggested that longitudinal dissociation and concealed reentry in the AV node occurred in atypical Wenckebach periods of variants II and III, but not in the other periods.     

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.     

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.     

Evidence suggesting dual A-V nodal pathways in patients without supraventricular tachycardias.

Electrophysiologic evidence for dual pathways of conduction through the A-V node is presented in three patients without history of supraventricular tachycardia. In case 1, abrupt spontaneous changes in the PR interval from 0.17 to 0.42 second were seen. His bundle electrographic studies showed two sets of A-H intervals during sinus rhythm and at several atrial pacing rates, although at rates over 100 per minute only the slow pathway conducted. Using the extrastimulus method, different refractory periods for the fast and slow pathways were documented. Cases 2 and 3 underwent His bundle electrography studies to evaluate intraventricular conduction defects. During atrial pacing studies abrupt changes in the A-H interval, from 220 to 470 msec and from 220 to 370 msec, were observed on increasing the pacing rate from 90 to 95 per minute in case 2 and from 120 to 130 per minute in case 3. In these two patients, dual A-V nodal pathways were suggested by the sudden changes in the A-H -interval at critical pacing rates. These findings indicate that evidence suggesting dual pathways of conduction through the A-V node may not be an uncommon finding and may be present without the manifestation of recurrent supraventricular tachycardias.     

Simultaneous anterograde fast-slow atrioventricular nodal pathway conduction after procainamide

Three patients with paroxysmal supraventricular tachycardia underwent electrophysiologic studies that included His bundle recordings, incremental atrial and ventricular pacing and extrastimulation before and after intravenous infusion of 500 mg of procainamide. In all three patients the tachycardia was induced during atrial pacing or premature atrial stimulation, or both. Two of the three patients had discontinuous atrioventricular (A-V) nodal curves with induction of a slow-fast tachycardia during failure in anterograde fast pathway conduction and one patient had a smooth A-V nodal curve with induction of a slow-fast tachycardia at critical A-H interval delays. After procainamide: (1) in all three patients atrial pacing induced A-V nodal Wenckebach periodicity (cycle length 300 to 400 ms) resulting in simultaneous anterograde fast and slow pathway conduction (one atrial beat resulting in two QRS complexes) and retrograde fast pathway conduction initiating an echo response or a slow-fast tachycardia, or both; (2) in all three patients there was enhanced conduction and shortening of refractoriness of the anterograde fast pathway and depressed conduction and lengthening of refractoriness of the retrograde fast pathway; and (3) in two patients there was inability to sustain tachycardia because of selective block within the retrograde fast pathway. In conclusion: (1) procainamide altered conduction and refractoriness of the anterograde fast and slow pathways so that simultaneous conduction could occur during atrial pacing, resulting in a double ventricular response and a slow-fast echo or tachycardia, or both; and (2) the differential effects of procainamide on anterograde fast and retrograde fast pathways suggests two functional A-V nodal fast pathways, one for anterograde and the other for retrograde conduction.     

Two-to-one A-V block with four-to-three A-V nodal wenckebach, a form of spontaneous multilevel block

Electrophysiologic studies in one patient with spontaneous 2:1 atrioventricular block and variable PR intervals revealed two sites of conduction block. Typical 4:3 A-V nodal Wenckebach was present in addition to Mobitz type II infra-His block. The HV of conducted complexes was 120 msec and the shortest recorded AH interval was 250 msec. When 2:1 A-V block with fixed PR interval was present, only 2:1 Mobitz type II infra His-block was present. The mechanism of this example of spontaneous multilevel A-V block is discussed and compared to other previously reported cases.     

Atypical atrioventricular Wenckebach periodicity caused by conduction through triple atrioventricular junctional pathway as a probable mechanism

Electrocardiograms were taken from an 84-year-old man with right bundle branch block in whom atypical atrioventricular Wenckebach periodicity was frequently occurred. The electrocardiographic findings as mentioned below suggested that the atypical periodicity was caused by conduction through triple atrioventricular junctional pathways as a probable mechanism. When a P wave was blocked after a markedly prolonged PR interval of 0.64 s, the RP interval containing this blocked P wave ranged between 0.84 s and 0.86 s, and the next P wave was followed by a QRS complex of the same configuration, with the PR interval of 0.35 s. On the other hand, when a P wave was blocked after a PR interval of 0.49 s or 0.52 s, the RP interval containing this blocked P wave was comparatively long, ie, 0.95 s or 0.98 s, and the next P wave was followed by a QRS complex of somewhat different configuration showing borderline left axis deviation, with a shorter PR interval of 0.21 s or 0.23 s. These findings suggest that longitudinal dissociation occurred not only in the atrioventricular junction but also in the His bundle. This is the first report suggesting triple atrioventricular junctional pathways probably associated with longitudinal dissociation in the His bundle.     

Periodic variation in atrioventricular conduction time: Mechanisms of initiation,maintenance and termination of periods of long PR intervals

Five patients with periodic variation in atrioventricular (AV) conduction time are reported in whom periods of comparatively short PR intervals alternated with periods of comparatively long PR intervals. In all patients, the transition from a period of long PR intervals to a period of short PR intervals usually occurred without a blocked P wave. In 3 patients, however, the period of long PR intervals was occasionally terminated by a blocked P wave. The mechanisms of initiation, maintenance and termination of periods of long PR intervals are explained by the use of dual AV pathways consisting of fast and slow pathways. It is suggested that the effective refractory period of the fast pathway was abnormally prolonged by increased vagal tone and that, during the period of long P-R intervals, sinus impulses anterogradely passed only through the slow pathway and later retrogradely excited the fast pathway. Apparently, when vagal tone was decreased, the effective refractory period of the fast pathway was shortened, resulting in abrupt improvement in atrioventricular conduction without a blocked P wave.     

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.     

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.     

Advanced A-V block with apparent A-V junctional escape complexes because of dual A-V nodal pathways

We report a patient with second degree A-V block in whom several sinus impulses were conducted over the slow A-V nodal pathway, resulting in P-R intervals so prolonged to suggest a diagnosis of intermittent advanced A-V block with A-V junctional escape complexes. However, the "escape" cycles were markedly irregular, and moreover, "escape" complexes often occurred with R-R cycles shorter than those ended by conducted sinus beats. These observations suggested that no escape mechanism was present. The marked variability of P-R intervals was a manifestation of dual A-V nodal pathways: short P-R intervals expressed conduction over the fast pathway, whereas long P-R intervals corresponded to sinus impulses conducted over the slow pathway.     

Incidence of 'dual A-V nodal pathways' in first- and second-degree type I supra-His A-V block

The incidence of ‘dual A-V nodal pathways’, diagnosedon the basis of spontaneous or induced modifications in thePR interval, has been assessed in a group of168 consecutivepatients with first- (77) and second-degree (91) type I supra-Hisblock.‘ Dual A-V nodal pathways’ were found in 12cases (16%) with first-degree and in 7 cases (7–7%) withsecond-degree type I supra-His A-V block. His bundle recordingconfirmed the hypothesis that PR interval variations observedin these cases are due to modifications in the AH interval andthus to changes in A-V nodal conduction velocity. The electrophysiologicstudy also showed that the phenomenon was easily reproducedby atrial stimulation. The frequent association between ‘dualA-V nodal pathways’ and supra-His blocks suggests thatthe block mechanism should be studied in depth as it could haveprognostic and therapeutic implications.     

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.     

Reciprocal rhythm in patients with normal electrocardiogram: Evidence for dual conduction pathways.

The present study refers to six patients in whom an A-V reciprocal rhythm could be documented; in four cases it took the form of sustained tachycardia. None of the patients showed any ECG feature of ventricular pre-excitation (PR interval of more than 0.12 sec. and normal QRS configuration). The extrastimulus method showed, at first, that the A-V conduction time of the premature beat varied only slightly with the decrease of the coupling interval. From a critical A1A2 interval there was a sudden lengthening of A2H2 preceding the occurrence of re-entrant beats. The curve of H1H2 responses reflected these changes, showing two distinct parts. The second part following the slowing of the impulse included the initiation zone of atrial echoes and of reciprocating tachycardia. These results suggest the existence of two A-V pathways, one fast and the other slow. The point at which the break between the two parts of the curve occurred might be related to the effective refractory period of the fast pathway. In the same way, when atrial pacing reached a critical rate, it induced an abrupt increase of AH in five cases. In the sixth patient, A-V conduction time remained unchanged up to 170 per minute. Ventriculoatrial conduction was always observed, the delay of which did not lengthen with the rate. In one case tachycardia could be induced by a premature ventricular beat without lengthening of the V-A time. It is concluded that in spite of a normal PR interval, the presence of dual A-V pathways may be implied in the genesis of reciprocal rhythm.     

The incidence of typical and atypical A-V Wenckebach periodicity

The classic pattern of the typical WP's consists of (1) progressive lengthening of the P-R intervals with the largest increment occurring in the second conducted beat, (2) progressive decrease in P-R increment which accounts for the progressive shortening of successive R-R intervals, and (3) the pause produced by the nonconducted P-wave is less than two P-P intervals. In 45 patients with atrial pacing-induced Wenckebach periods of A-V conduction, the structure of these was studied with His bundle recordings. Of the 128 periods analyzed exceeding 3:2 A-V conduction ratios, 66 per cent were atypical. In 24 patients with spontaneous WP's of A-V coduction, the electrocardiographic records were studied. Of the 98 periods analyzed exceeding 3:2 A-V conduction ratios, 86 per cent were atypical. WP's with A-V conduction ratios greater than 6:5 were all atypical. Five categories of atypical WP's are described.     

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.     

Atypical Wenckebach periodicity simulating Mobitz II AV block.

Eleven patients were studied and a total of 144 Wenckebach cycles in the AV node and 118 Wenckebach cycles in the His-Purkinje system were analysed to determine the incidence of typical and atypical Wenckebach periodicity, with particular emphasis on one variant of atypical Wenckebach that may simulate a Mobitz type II block. This pseudo-Mobitz II pattern was defined as a long Wenckebach cycle in which, at least, the last three beats of the cycle show relatively constant PR intervals (variation of no more than 0.02 s in surface leads and no more than 10 ms in His bundle electrograms) and in which the PR interval immediately following the blocked beat is shorter than the PR interval before the block by 0.04 s or more. Atypical Wenckebach cycles were found to be more common than the typical variety at both the AV node (67%) and His-Purkinje system (69%). The pseudo-Mobitz II pattern was seen in 19 per cent of atypical AV nodal Wenckebach periods and in 17 per cent of atypical His-Purkinje system Wenckebach cycles. The need to discern a ''classical'' Mobitz II block from a pseudo-Mobitz II pattern, especially in the setting of an acute inferior myocardial infarction, is emphasised.     

Alternating reversed wenckebach periodicity: Concealed electrotonic conduction as a possible mechanism

Electrocardiograms were taken from a 67-year-old man with 2:1 atrioventricular block in whom alternating reversed Wenckebach periodicity was found. Long PR intervals of alternately conducted P waves progressively shortened until an alternate P wave was blocked. After an alternate P wave was blocked, the next alternate P wave was conducted to the ventricles with a markedly long PR interval. Then long PR intervals of alternately conducted P waves progressively shortened again until an alternate P wave was blocked. This is the first report on alternating reversed Wenckebach periodicity. It seems that concealed electrotonic conduction of alternately blocked impulses occurred as a possible mechanism.     

Paradoxical Shortening of the Second PR Interval During 3:2 Atrioventricular Nodal Block

Paradoxical Shortening in Second-Degree AV Block. A patient with 3:2 second-degree AV block after acute inferior wall myocardial infarction showed consistent PR interval shortening on the second conducted beat in each periodicity. Intracardiac electrophysiologic evaluation revealed that the site of block was nodal. A typical Wenckebach pattern with prolongation of the AH interval was noted. The shorter PR resulted from a paradoxical shortening of the HV interval in the second beat, most likely due to supernormal conduction in the setting of concomitant trifascicular disease.     

Intermittent pseudocomplete A-V block due to A-V dissociation in presence of 2:1 A-V block.

A false pattern of intermittent complete A-V block was seen in two asymptomatic patients when A-V dissociation was superimposed on a basic 2:1 A-V block. Although the conduction disturbance occurred at the A-V nodal level in both cases, in Case 2 it resembled A-V block due to bilateral or trifascicular disease. This arrhythmia was the end result of Type I (Wenckebach) block and apparently has a better prognosis than those emerging from a Type II (Mobitz) block.