Existence of automaticity in anomalous bundle of Wolff-Parkinson-White syndrome

Escape beats probably arising from the anomalous bundle were documented in 2 patients with the Wolff-Parkinson-White (WPW) syndrome. A third patient, in whom complete AV block developed both in the anomalous bundle and the normal pathway, showed the occurrence of escape beats (an escape-bigeminy pattern), as well as a regular idioventricular rhythm arising from the anomalous bundle. Phase 4 block in the anomalous bundle occurred in 7 other patients, in 4 of them spontaneously and in 3 only after the administration of ajmaline or amiodarone. Only 4 of 14 fully investigated patients (out of a total number of 23) showed absence of both escape beats and phase 4 block. The escape beats were considered as direct evidence, and the phase 4 block as indirect evidence, for the existence of automaticity in the anomalous bundle. Such evidence supports the view that the anomalous bundle, like the His bundle-branch system, may be composed of specialised tissue endowed with the property of automaticity.     

Electrophysiologic and pharmacologic studies in a patient with acute myocardial infarction complicated by intraventricular and atrioventricular block.

A patient with an acute anterior wall myocardial infarction complicated by bilateral bundle branch block and paroxysmal AV block is presented. The following new, uncommon or unreported phenomena were documented: the simultaneous occurrence of phase-3 block in the right bundle branch and phase-4 block in the left bundle branch; the simultaneous occurrence of phase-4 block in both main bundle branches; phase-4 left posterior hemiblock associated with escape beats arising from the injured posterior division of the left bundle branch; supernormal conduction in the right bundle branck and 2:1 right bundle branch block related to supernormality. Most of these changes were, of course, not simultaneous, and their successive appearance was related to day-to-day and sometimes hour-to-hour variations in the degree and quality of the multifascicular injury caused by the infarct. In addition, the actions of several drugs upon automaticity and conduction were tested. The effects of amiodarone, lidocaine and isoproterenol were similar to those previously reported under comparable circumstances. At a moment when the patient had repeated episodes of paroxysmal AV block with severe Adams-Stokes seizures, the administration of a single i.v. dose of 0.25 mg of strophanthin suppressed totally the Adams-Stokes attacks through a significant enhancement of ventricular automaticity. If rapid implantation of an artifical pacemaker is not at hand, strophanthin may be life-saving in patients with acute paroxysmal AV block.     

Mechanism and significance of widened QRS complexes during complete atrioventricular block in acute inferior myocardial infarction

Twelve of 35 consecutive patients admitted with complete, atrioventricular (A-V) block complicating acute inferior myocardial infarction manifested widened QRS complexes. The escape beats had the pattern of left bundle branch block in four patients, right bundle branch block in five patients and both left and right bundle branch block in three patients.

His bundle recordings in five patients with escape beats that had a left bundle branch block configuration revealed a His bundle potential preceding the widened QRS complex at His-V intervals of 45 to 60 msec. Bradycardia-dependent left bundle branch block was demonstrated in two patients by His bundle pacing. In three patients the conducted beats had a left bundle branch block configuration after critical lengthening of the R-R interval during second degree A-V block before or after the episode of complete A-V block. In six patients whose escape beats had a right bundle branch block configuration, His bundle recordings did not reveal a His bundle potential preceding these beats.

Our observations suggest that widened QRS complexes with a left bundle branch block configuration could be due to an A-V junctional escape rhythm with phase 4 left bundle branch block. Alternatively in association with a right bundle branch block configuration it is possible that the widened QRS complexes represent a ventricular or fascicular escape rhythm.

Two of 12 patients with widened QRS complexes died. There were no significant differences in immediate mortality, 6 month mortality or mean peak serum glutamic oxaloacetic transaminase (SGOT) values between patients with narrow and widened QRS complexes. This finding suggests that widened QRS complexes during complete A-V block in acute inferior myocardial infarction have no prognostic significance.     

Pseudo bundle branch block produced by premature impulses arising in the bundle branches.

Pseudo bundle branch block, a previously unreported arrhythmia produced by concealed premature impulses arising in the bundle branches, was seen in two patients with sick sinus node syndrome. Although concealed conduction was not apparent in either the surface or intracardiac leads, the latter were essential in localizing the site of manifest impulse formation. Patient 1, with left bundle branch extrasystoles, had pseudo bundle branch block and pseudo atrioventricular block that depended on the timing and extent of concealment of premature depolarization. Because of the coexisting sinus bradycardia in this patient, electrical stimulation and the recording of the right ventricular apical electrograms gave additional information that helped corroborate the postulated mechanisms. Patient 2 had right bundle branch extrasystoles with sinus beats that showed a right bundle branch block pattern possibly caused by pseudo bundle branch block. In this case the possibility that both the automaticity and the conduction disturbance had a mechanical origin could not be excluded.     

Automaticity of the Kent bundle: confirmation by phase 3 and phase 4 block

Automaticity in the Kent anomalous atrioventricular bundle has been postulated to occur on the basis of electrocardiographic recordings. This hypothesis was confirmed using intracardiac recordings and programmed stimulation in a patient with pre-excitation. It was supported, in part, by demonstrating the presence of phase 3 and phase 4 block in the Kent bundle during decremental atrial pacing. The existence of automaticity in the Kent bundle may explain the manifestation of intermittent pre-excitation in certain patients. Furthermore, the presence of phase 3 and phase 4 block makes the likelihood of rapid antidromic conduction over the Kent bundle pathway unlikely within this subgroup.     

Effect of procainamide and lidocaine on ventricular automaticity and reentry during acute coronary occlusion

A model was developed to study ventricular automaticity and reentry in the heart of open chest dogs during myocardlal ischemia. Atrioventricular (A-V) block and the resultant idioventricular rhythm were induced by surgical destruction of the His bundle, and acute myocardial ischemia was produced by ligation of the left anterior descending coronary artery. The ventricle was paced by basic stimuli, and one or two premature beats were introduced at various coupling Intervals after the 10th basic beat. Two different types of response to these premature beats could be observed: (1) rapidly repetitive beats or fibrillation due to reentry after early premature beats, and (2) the appearance of escape beats from idioventricular automatic fibers after late premature beats.With this model of ventricular reentry and automaticity, the effect of procainamide (group I antiarrhythmic agent) was studied in 12 dogs, and that of lidocaine (group II) in 13 dogs. Both procainamide and lidocaine were effective in decreasing automaticity since they significantly increased postextrasystolic escape intervals of idloventricular beats. Although procainamide failed to abolish the reentrant beats induced by early premature beats in all 12 dogs, lidocaine abolished these beats in 10 of 13 dogs. The results indicate that lidocaine is much more effective than procainamide in preventing ventricular reentrant activity induced by early premature beats.     

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.     

Repetitive supernormal conduction in the right bundle branch in high degree bilateral bundle branch block

Electrocardiograms were taken from a 67-year-old woman with high-degree atrioventricular block in which ventricular escape beats of right bundle branch block pattern occurred, accompanying occasional ventricular capture beats. Only when a sinus P wave occurred 0.60 s after the preceding escape beat, it was followed by a capture beat of left bundle branch block pattern with the RP interval of 0.60 s and the PR interval of 0.19 s. Similar left bundle branch block with left axis deviation pattern had been shown in the electrocardiogram taken 2 years before. Such RP and PR intervals in capture beats were invariable. These suggest that capture beats occurred as a result of supernormal conduction in the right bundle branch, which denies the possibility of ventricular extrasystoles. Such capture beats with the above RP and PR intervals were observed repeatedly.     

Chronic His bundle block. Clinical, electrocardiographic, electrophysiological, and follow-up studies on 16 patients.

This report describes 16 patients with block within the His bundle seen over a period of 55 months. Ten were women and 6 men, with an average age of 76 years, range, 42 to 98 years. All patients had His bundle recordings showing split His bundle potentials (H and H) (13 patients) or narrow QRS with block distal to the His bundle potential (3 patients). Of the 16 patients, 10 had complete heart block, 4 second degree AV block (2 patients with Mobitz type II, and 2 with 2:1), and 2 first degree AV block. Ten patients had a narrow QRS in the conducted beats or escape rhythms. Intravenous atropine (1 to 2 mg) had a variable effect on AV conduction and the rate of the escape rhythm. Twelve patients have had a permanent pacemaker implanted. During the follow-up period, 10 patients died 1 to 31 months from the time of initial examination. The remaining 6 patients (5 with pacemaker) are alive 3 to 58 months later.     

Concealed nonparoxysmal junctional tachycardia.

Electrophysiologic studies were performed in a patient who had an apparently uncomplicated complete trifascicular block. His bundle recordings revealed atrioventricular dissociation with: 1) an atrial rate of 58 beats/min, 2) an idioventricular escape rate of 45 beats/min, and 3) nonparoxysmal junctional tachycardia (His bundle rhythm) at a rate of 65--85 beats/min. The latter arrhythmia was electrocardiographically silent, influencing neither atrial nor ventricular events. The arrhythmia probably reflected digitalis intoxication (digoxin level of 3.3 ng/ml). A repeat electrophysiologic study 4 days after digoxin was discontinued revealed complete trifascicular block (distal to H) with intact conduction between the atrium and the His bundle (AH of 150 msec). Thus, electrophysiologic study demonstrated an electrocardiographically silent but clinically relevant arrhythmia, suggesting that His bundle recording should be part of diagnostic study during temporary pacemaker implantation in patients with atrioventricular block.     

Mahaim conduction producing left axis deviation and normal QRS.

An unusual patient is described in whom electrophysiological studies strongly suggest the occurrence of Mahaim conduction. The patient whose electrocardiogram previously showed a left anterior hemiblock pattern then developed advanced atrioventricular (AV) block (AH block). Beats conducted through the atrioventricular node always had a short HV interval (20 ms) and QRS complexes of left anterior hemiblock pattern. Junctional escape beats always had a normal HV interval (50 ms) with normal intraventricular conduction. His bundle pacing showed the StV interval and QRS contour of escape beats. These findings suggest the existence of an accessory pathway (Mahaim fibres) passing from the area of block, presumably the uppermost portion of the His bundle, to the posteroinferior division of the left bundle-branch. The surface electrocardiogram did not show the characteristic delta wave of the Wolff-Parkinson-White syndrome. Our observations suggest that patients in whom there is conduction along Mahaim fibres may show only the pattern of intraventricular conduction defect without a delta wave.     

Mahaim conduction producing left axis deviation and normal QRS.

An unusual patient is described in whom electrophysiological studies strongly suggest the occurrence of Mahaim conduction. The patient whose electrocardiogram previously showed a left anterior hemiblock pattern then developed advanced atrioventricular (AV) block (AH block). Beats conducted through the atrioventricular node always had a short HV interval (20 ms) and QRS complexes of left anterior hemiblock pattern. Junctional escape beats always had a normal HV interval (50 ms) with normal intraventricular conduction. His bundle pacing showed the StV interval and QRS contour of escape beats. These findings suggest the existence of an accessory pathway (Mahaim fibres) passing from the area of block, presumably the uppermost portion of the His bundle, to the posteroinferior division of the left bundle-branch. The surface electrocardiogram did not show the characteristic delta wave of the Wolff-Parkinson-White syndrome. Our observations suggest that patients in whom there is conduction along Mahaim fibres may show only the pattern of intraventricular conduction defect without a delta wave.     

Effect of ventricular premature beats on idioventricular pacemaker activity

The effect of ventricular premature beats on idioventricular pacemaker activity was studied in open-chest dog hearts with a surgically induced block in the His bundle. While the ventricle was paced by basic stimuli at a given rate, the pacing was interrupted for about 2.5 seconds following every twelfth basic beat (V₁) in order to obtain the interval between V₁ and the first escape beat (V_e) or the basic escape interval (V₁V_e). Ventricular premature beats (V₂) were then introduced at various coupling intervals (V₁V₂) and the effect of these premature beats on the postextrasystolic escape interval (V₁V_e) was observed. The plot of V₂V_e against V₁V₂ intervals showed that the V₂V_e interval was shortest at shorter V₁V₂ intervals, and it increased gradually with the increase in V₁V₂ intervals. The V₂V_e intervals at shorter coupling intervals were much shorter than the basic escape interval (V₁V_e), indicating enhanced automaticity after early premature beats. The V₂V_e at longer coupling intervals were much longer than the basic escape intervals, indicating suppressed automaticity after late premature beats. The similar response to ventricular premature beats was noted during spontaneous idioventricular rhythm. The suppression was more pronounced at faster pacing rates and following two successive premature beats, probably due to the phenomenon of overdrive suppression. The same phenomena of altered automaticity after premature beats could be observed under the influence of ouabain, epinephrine, lidocaine, and propranolol, although these agents either decreased or increased the average escape intervals. The results may explain the clinically observed alteration of the idioventricular pacemaker rate following ventricular premature beats.     

Contrasting effects of verapamil and procainamide on rate-dependent bundle branch block: pharmacologic evidence for the role of depressed sodium channel responses

The mechanisms responsible for intermittent bundle branch block are still under debate. The role of the time-dependent behavior of the slow calcium channel has recently been emphasized. To test this hypothesis and ascertain the possible involvement of the fast sodium channel, the effects of the slow calcium channel blocker verapamil and the fast sodium channel blocker procainamide were compared in 10 patients with intermittent bundle branch block. All 10 patients showed bundle branch block during spontaneous sinus rhythm. Maneuvers to slow cardiac rate (that is, carotid sinus massage, Valsalva maneuver) were performed to identify normal conduction as well as phase 4 bundle branch block. Thus, the ranges of diastolic intervals (RR) resulting in phase 3 (tachycardia-dependent) bundle branch block, phase 4 (bradycardia-dependent) bundle branch block and normal conduction were measured in two control studies performed before intravenous administration of verapamil (control 1) and procainamide (control 2) and at the peak effect of both drugs. In the control studies, all 10 patients showed phase 3 bundle branch block, whereas phase 4 bundle branch block occurred in only 4 patients. The ranges of phase 3 bundle branch block, phase 4 bundle branch block and normal conduction were very similar in control studies 1 and 2. The phase 3 bundle branch block range was slightly shortened by verapamil (983 +/- 83.5 ms in control 1; 930 +/- 69.4 ms at the peak effect of verapamil), whereas phase 4 bundle branch block remained unchanged. In contrast, conduction was systematically worsened by procainamide.(ABSTRACT TRUNCATED AT 250 WORDS)     

Bundle branch block in alternate beats during 2:1 atrial flutter

This presentation deals with a case of atrial flutter. During 2:1 A/V conduction, the QRS complexes showed a regular alternation of narrow beats and wide beats with a typical configuration of left bundle branch block. In contrast, pauses resulting from 4:1 A/V conduction ratio always resulted in narrow beats. Disappearance of left bundle branch block with long R-R intervals demonstrated that the block was tachycardia-dependent or phase 3. Analysis of the tracing suggested that narrowing of QRS complexes in alternate beats was due to supernormal left bundle branch conduction associated with retrograde concealed conduction into the anterogradely blocked bundle branch.     

Selective Atrionodal Input Ablation for Induction of Proximal Complete Heart Block with Stable Junctional Escape Rhythm in Patients with Uncontrolled Atrial Fibrillation

Background: The study tests the hypothesis that ablating all inputs to the atrioventricular (AV) node can result in complete heart block with stable junctional escape rhythm. Methods and Results: We attempted atrionodal input ablation in 76 consecutive patients with uncontrolled atrial fibrillation. Fast and slow pathways were first ablated. If there was no AV block, additional energy applications were done between fast and slow pathway locations. The patients were followed for 42 ± 11 months. Group I (n = 57) comprised patients with complete heart block and junctional escape rhythm (53 ± 4 beats/min) at the end of the procedure. The escape rhythm remained stable throughout follow-up. Group II (n = 15) were patients who failed the stepwise atrionodal input ablation and required AV junctional ablation guided by His bundle potential to achieve complete heart block. Four patients showed a slow escape rhythm after ablation (33 ± 4 beats/min). Others had no escape rhythm. All 15 pts remained pacemaker dependant. The total death rate of groups I and II was 18/57 (31.6%) vs 10/15 (66.7%), respectively (p < 0.02). These differences could not be explained by a difference of left ventricular ejection fraction (0.42 ± 0.07 vs 0.41 ± 0.04, respectively, p = NS). Conclusions: (1) In most patients, ablation of both fast and slow pathways did not result in complete heart block, indicating the presence of multiple atrionodal inputs. (2) Ablation of all atrionodal inputs may result in complete heart block with stable junctional escape rhythm. (3) As compared with AV junctional ablation, atrionodal input ablation was associated with a lower mortality rate on long-term follow up.     

Clinical and electrocardiographic features and long-term results of electrical therapy in patients with isolated His bundle disease

The clinical, ECG, and electrophysiologic findings of 35 consecutive patients with second- and third-degree intra-His block with normal QRS complexes were examined. The follow-up period varied between 12 and 120 months (mean 45). Seventy-seven per cent of the patients were women. Underlying heart disease was present in 43% of the patients. ECGs were characterized by both second-degree type I and type II atrioventricular block, normal or slightly prolonged PR interval of the conducted beats or of the first conducted beat of a Wenckebach sequence, and by subtle changes in the initial forces of the QRS complexes of the escape beats. Electrophysiologic study showed normal sinus and atrioventricular node function and normal infra-His conduction in all patients. In four patients repetitive bradycardia-dependent intra-His block was induced. Thirty-two patients were permanently paced soon after the initial evaluation and three during the follow-up period. Total long-term mortality rate was 23%. None of the patients developed bundle branch block.     

Premature escape beats induced by overdrive pacing in canine Purkinje fibers. Evidence for the role of normal automaticity as an underlying cellular mechanism.

Premature escape beats induced in conscious dogs with chronic complete atrioventricular block have been defined as escape beats occurring on cessation of overdrive pacing and having a coupling interval to the last paced beat shorter than the coupling interval between the premature escape beat and the second postpacing beat. Triggered activity has been proposed as the primary underlying mechanism. We used standard microelectrode techniques to study the effects of overdrive pacing on normal automatic canine Purkinje fibers to determine if premature escape beats could be induced and if so, to define the underlying cellular mechanism(s). For this purpose, we overdrive-paced Purkinje fibers for 10 and 50 seconds and for 10 and 50 beats at a pacing cycle length (PCL) of 1,000-200 msec. In addition, to help distinguish among major arrhythmogenic mechanisms, we used a matrix of drugs consisting of propranolol, nadolol, lidocaine, ethmozin, and doxorubicin. Fifty-second stimulation trains induced "classic" overdrive suppression of the first three postpacing impulses, whereas 10-second overdrive pacing induced significant overdrive suppression only at a PCL of 200 msec. With 50-beat overdrive pacing and a PCL of 1,000-600 msec, there was overdrive suppression of postpacing impulses, whereas reduced overdrive suppression was observed at a PCL of 400-200 msec. Ten-beat stimulation trains induced a "flat response" of postpacing impulses. Ten- and 50-beat overdrive pacing provoked premature escape beats in 66% of the fibers, with the higher incidence at a PCL of 200 msec for 50-beat stimulation trains. No shortening of the coupling interval of premature escape beats was observed at faster pacing rates. Only lidocaine (which suppresses normal automaticity) abolished premature escape beats. We conclude that normal automaticity is the most likely mechanism underlying premature escape beats in Purkinje fibers with high levels of membrane potential.