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.     

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.     

Wide complex tachycardia with atrioventricular dissociation and QRS morphology identical to that of sinus rhythm: a manifestation of bundle branch reentry.

OBJECTIVE: To determine the features that distinguish bundle branch reentry (BBR) ventricular tachycardia from a supraventricular tachycardia with aberration on the 12 lead electrocardiogram (ECG). PATIENTS: Three patients in whom premature beats (2 cases) or sustained tachycardia (2 cases) showed a QRS configuration identical to that observed during sinus rhythm. INTERVENTIONS: Programmed electrical stimulation. RESULTS: These arrhythmias were ventricular in origin and caused by a BBR mechanism, as suggested by the following data obtained during electrophysiological study: (a) an H-V interval shorter during tachycardia than during sinus rhythm; (b) A-V dissociation; (c) activation of the right bundle branch before activation of the bundle of His. The ECG of all 3 patients showed right bundle branch block with very prolonged QRS duration (0.16 to 0.20 s). Characteristically, all 3 had prolonged H-V interval during sinus rhythm. All patients had had a previous myocardial infarction and had a dilated left ventricle. CONCLUSION: The presence of (a) wide complex extrasystoles or tachycardia with a QRS morphology identical to that of sinus rhythm; (b) A-V dissociation; and (c) a very prolonged QRS duration (0.16 s or more) is suggestive of ventricular tachycardia caused by bundle branch reentry.     

Observations in patients showing A-V junctional echoes with a shorter P-R than R-P interval: Distinction between intranodal reentry or reentry using an accessory pathway with a long conduction time

Single test stimulation of the ventricle revealed initiation of echoes with a supraventricular QRS complex with a shorter P-R than R-P interval in 28 of 300 patients consecutively studied with programmed electrical stimulation of the heart because of documented or suspected tachycardias. In all 28 the initiation of echoes was related to a discontinuity in the retrograde conduction curve. In 10 patients a different atrial activation sequence in the endocavitary leads was present before and after the discontinuity in the retrograde conduction curve. In five of these a sustained tachycardia with a shorter P-R than R-P interval could be initiated, and in all five patients an accessory pathway with a long conduction time as the retrograde arm of the tachycardia circuit could be demonstrated. In these five patients spontaneous initiation of tachycardia was observed during sinus rhythm or after atrial premature beats. Tachycardia accelerated after the administration of atropine. In the remaining 23 patients the initiation of echoes showing a shorter P-R than R-P interval was nonsustained. In these patients spontaneous initiation of such echoes during sinus rhythm or initiation by atrial premature beats was not observed, and echoes with this relation of the P-R and R-P intervals systematically disappeared after administration of atropine.It is postulated that in these patients a slow atrioventricular (A-V) nodal pathway is used in the retrograde direction during echoes showing a shorter P-R than R-P interval. Sustained A-V junctional tachycardia showing this relation between P-R and R-P intervals favors incorporation of an accessory pathway with slow retrograde conduction in the tachycardia circuit.     

Influence of sinus impulses on the parasystolic cycle length

Recently, it has been shown that in most clinical cases of parasystole, the parasystolic rhythm is not completely independent of the sinus rhythm. In this study, to disclose the mechanism of such "irregular" parasystole, parasystolic cycles with an intervening sinus QRS complex (XSX) were compared with their immediately adjacent pure parasystolic cycles without any intervening nonparasystolic QRS complexes (XX) in 10 cases of ventricular parasystole. In eight cases, the XSX interval was equal to or nearly equal to the adjacent pure XX interval; in one, the XSX interval was shorter than the XX interval; and in only one, the XSX interval was longer than the XX interval. In six cases in which the XSX interval was almost equal to the XX interval, calculated XSX intervals with a later intervening sinus QRS complex were obtained from the differences between the XSSX interval (ie, interectopic interval with two intervening sinus QRS complexes) and its adjacent XX interval. In five of the six cases, the calculated XSX interval was shorter than the XX interval. These observations suggest that in most cases of parasystole, early intervening sinus impulses do not change the parasystolic cycle, whereas late intervening sinus impulses shorten the parasystolic cycle. This suggests the presence of type I second-degree entrance block as the mechanism of "irregular" parasystole.     

Familial atrioventricular heart block; an autosomal dominant trait.

A family of 28 individuals spanning four generations was investigated because of a finding of complete heart block in five members and the existence of a low degree of atrioventricular (A-V) heart block in a sixth member. The disorder was characterized by 1) adult onset in all, 2) complete A-V heart block in five and first degree A-V heart block in one, 3) sinus bradycardia in three, 4) atrial fibrillation in five, 5) abnormal QRS complex in five, 6) ventricular tachycardia in three, 7) left ventricular enlargement in all, and 8) mitral insufficiency in five. Proximal location of the A-V heart block was suggested by the fact that atropine caused acceleration of the ventricular rate and by the presence of a His bundle potential preceding the QRS complexes. Involvement of the distal conducting system was indicated by the widened QRS complex and a prolonged H-V interval. Pathologic examination in one case showed extensive sinus node fibrosis and interruption of the A-V node-His bundle connection. This disorder is probably due to an autosomal dominant trait.     

Manifest and concealed AV nodal reentry in wenckebach type of AV conduction with AV junctional escape rhythm

An electrocardiogram was obtained that was characterized by sinus rhythm with progressive prolongation of the PR interval not followed by a blocked sinus impulse. After a critically long PR interval, the QRS complex was followed by a premature P′ wave, representing an echo beat, a manifest reentry in the atrioventricular (AV) node. The pause, occasioned by the premature P′ wave, was at times interrupted by an AV junctional escape beat, occurring with an escape interval of 1.21–1.24 seconds. On other occasions, however, the escape beat did not manifest on schedule, even though the pause was markedly longer than the escape cycle. This suggested that the manifest reentry was followed by a further concealed reentry, resulting in inapparent discharge of the AV junctional escape pacemaker, whose firing was postponed, thereby allowing the sinus impulse to capture the ventricles.     

Onset of atrial fibrillation during antidromic tachycardia: Association with sudden cardiac arrest and ventricular fibrillation in a patient with Wolff-Parkinson-White syndrome

Electrophysiologic evaluation in an 18 year old youth with the Wolff-Parkinson-White syndrome who had a sudden cardiac arrest while playing racquetball revealed two types of paroxysmal reciprocating tachycardia: (1) A normal QRS tachycardia with a short ventriculoatrial (V-A) interval fulfilled the criteria for reentry within the atrioventricular (A-V) node; and (2) a wide QRS tachycardia with a QRS configuration of maximal preexcitation was demonstrated to be the result of an antidromic mechanism.During laboratory study, the wide QRS tachycardia spontaneously degenerated into atrial fibrillation. In the basal state, the shortest R-R interval between preexcited QRS complexes was 270 ms, but after infusion of isoproterenol (1.6 μg/min intravenously), the shortest R-R interval became 180 ms. Consequently, this electrophysiologic study suggested that evolution of antidromic reciprocating tachycardia into atrial fibrillation with a rapid ventricular response during exercise-induced catecholamine release may have been the mechanism for ventricular fibrillation in this patient.     

Mechanism of closure of the mitral prosthetic valve and the role of atrial systole. Phonocardiographic and cinefluorographic study

Phonocardiographic and Cinefluorographic methods were used to study the mechanism of closure of the Starr-Edwards mitral prosthetic valve (model 6320) in 41 patients with a normal QRS interval. Atrial fibrillation was present in 23 patients and normal sinus rhythm in 18. The following intervals were measured: QRS to mitral closing click (Q-Mc), QRS to onset of closure (Q-Oc) and QRS to completion of closure (Q-Cc) of the prosthetic valve. Ball travel time was measured as Q-Cc minus Q-Oc. Mean Q-Oc was shorter in the group with normal sinus rhythm. In 8 patients in this group, Q-Oc occurred before ventricular systole and, in 2, completion of closure occurred before the QRS interval. Early closure in the group with normal rhythm was related to a prolonged P-R interval. In this group, values for Q-Mc and Q-Cc intervals did not differ significantly. Q-Cc in the groups with atrial fibrillation and normal sinus rhythm were not significantly different. Ball travel time was significantly longer in the latter group. Long R-R intervals in the group with atrial fibrillation may be associated with partial and occasionally complete premature closure of the valve. Q-Mc was inversely related to the R-R interval in this group.This study indicates 3 mechanisms for closure of the mitral prosthetic valve. Atrial or ventricular contraction alone may close the valve. The contribution of each is dependent on the time interval separating the contraction of these chambers. Spontaneous partial or complete closure may occur before ventricular systole during a prolonged R-R interval.     

Electrophysiologic studies in the syndrome of short P-R interval, normal QRS complex

Eighteen subjects with a short P-R interval (<0.12 second) and normal QRS complex were studied by means of His bundle recordings and programmed atrial premature depolarizations. Eight subjects had a history of supraventricular tachycardia. During sinus rhythm, the A-H interval was less than or at the lower limits of normal values (45 to 80 msec), and the H-V interval was normal (30 to 50 msec). Atrial pacing at rates of up to 160/min produced 3 types of responses. Thirteen subjects showed a progressive increase in A-H interval similar to that of normal subjects but to a lesser degree. Three subjects showed an initial increase at low pacing rates, followed by a plateau response and further increase at higher rates. Two subjects showed no significant increase in the A-H interval. In 6 of 8 subjects with supraventricular tachycardia, atrial premature depolarizations produced atrial echo beats and sustained supraventricular tachycardia in 4, indicating atrioventricular (A-V) nodal reentry as the mechanism for the supraventricular tachycardia. In 10 subjects, refractory periods of the various components of the A-V conducting system were found to be similar to those of subjects with a normal P-R interval. The data suggest the following possible explanations for the short P-R interval: (1) total or partial bypass of the A-V node; (2) an anatomically small A-V node; (3) a short or rapidly conducting intranodal pathway; or (4) isorhythmic A-V dissociation.     

Electrophysiologic effects of pindolol on atrioventricular conduction in canine heart.

The effects of intravenous pindolol on the electrophysiologic properties of the atrioventricular conduction system was studied in intact dog, using His bundle electrogram and the extrastimulus method. Pindolol was administered intravenously in a dose range of 4 to 40 micrograms/Kg. The latter dosage of pindolol is above those used clinically. Significant effects of intravenous pindolol were observed on sinus cycle length, the A-V nodal conduction time, the ERP of the atrium, the ERP and FRP of the A-V node, and the ERP of the ventricle. Sinus cycle length was prolonged during sinus rhythm. Intraatrial conduction time was not altered by pindolol, while the ERP of the atrium was slightly increased. The A-H interval was generally prolonged by pindolol without Wenckebach type A-V block, but the H-V interval was unchanged. Both ERP and FRP of the A-V node was prolonged. The ERP and RRP of the His-Purkinje system were not statistically evaluated, because no block within the His-Purkinje system were not statistically evaluated, because no block with the His-Purkinje system or prolongation of H-V interval was produced and only a few QRS complexes by extrastimulus showed aberrant configration in the intact canine heart. In addition, pindolol prolonged the ERP of the ventricle.     

Spontaneous cardiac resynchronization

A 73-year-old woman with dilated cardiomyopathy presented with heart failure. The ECG showed sinus rhythm with left bundle branch block, left-axis deviation and prolonged QRS duration and frequent ventricular premature complexes from the left ventricular septal wall were present. Ventricular premature beats had narrower QRS duration than sinus node beats conducted through the His-purkinje fibers consistent with resynchronizing beats. The mechanisms of narrowing of the QRS complex produced by premature beats in cases of impaired intra and interventricular conduction are discussed.     

Effects of exercise and isoproterenol during atrial fibrillation in patients with wolff-parkinson-white syndrome

The effects of exercise and isoproterenol on atrial fibrillation (AF) were studied in 17 patients with Wolff-Parkinson-White syndrome (WPW) to assess the risk of developing a rapid ventricular response. Mean cycle length (R-R interval) and shortest R-R interval between both preexcited and nonpreexcited QRS complexes were recorded, as well as the percentage of preexcited complexes during control periods, during bicycle exercise, and during isoproterenol infusion. Exercise resulted in significantly shorter mean cycle length and the shortest R-R interval between nonpreexcited complexes. Exercise also resulted in a significantly lower percentage of preexcited complexes during AF, but had no effect on the R-R intervals between preexcited complexes. Isoproterenol had a variable effect on the percentage of preexcited QRS complexes, but resulted in significant shortening of mean cycle length and the shortest R-R interval between both normal and preexcited complexes. With isoproterenol, 12 of 17 patients had shortest preexcited R-R intervals ≤215 ms, compared with 6 of 17 in the control state. Isoproterenol infusion increased the rate of conduction over the accessory pathway during AF and allowed better assessment of the risk of excessively rapid rates occurring during AF. Exercise is not an adequate test for this purpose.     

Paroxysmal tachycardia with atrioventricular dissociation in a patient with a variant of pre-excitation syndrome

We report a patient with a variant of the pre-excitation syndrome who has paroxysmal tachycardia with a pattern of left bundle branch block and ventriculo-atrial dissociation. The tachycardia is precipitated by exercise, reproduced by atrial pacing and terminated with lidocaine. Between attacks the electrocardiogram revealed prominent R waves in right precordial leads and the vectorcardiogram displayed anterior displacement of the mean QRS vector, but neither was diagnostic of pre-excitation. The resting P-R interval (140 msec) and A-H interval (60 msec) were within normal limits, but the H-V interval (30 msec) was at or slightly below normal limits. Increasing heart rate from 80 to 150/min with atrial pacing increased A-H from 70 to 160 msec, but did not change the H-V interval. With pacing at 160/min, A-H lengthened progressively from 160 to 190 msec, but A-V remained constant at the critical limit of 190 msec. Accordingly, the H-V interval decreased until the His spike disappeared into the QRS or did not occur because of A-V block. At this point, the QRS complex changed to that seen during spontaneous tachycardia. Pacing was stopped, but tachycardia continued at 160/min and ventriculoatrial dissociation appeared. Lidocaine promptly restored sinus rhythm. We speculate that the patient has anomalous conduction between the lower segment of the A-V node and the ventricular septum (Mahaim fibers) and a reciprocating tachycardia which results from antegrade conduction down the anomalous pathway and retrograde conduction up the His-Purkinje system and lower A-V node. Ventriculo-atrial Wenckebach during the tachycardia excludes participation of atria and upper part of the A-V node in the re-entrant tachycardia. This variant of pre-excitation syndrome could easily be mistaken for “true ventricular tachycardia” and serious heart disease.     

His bundle recordings in a case of complete atrioventricular block combined with pre-excitation syndrome.

In a patient with complete A-V block suffering from attacks of dizziness an intermittent A-V conduction with a short P-R interval and a delta wave of the conducted ventricular complex were observed. After accelerating the sinus rate by atropine and by exercise, one-to-one conduction was established with QRS complexes of WPW type A configuration. His bundle recordings revealed a complete block within the normal conduction system at the level of the A-V node. A slow junctional rhythm with a normal H-V interval was activating the ventricle. During atrial pacing a one-to-one conduction through an accessory pathway could be documented at cycle lengths between 800 and 380 msec. sandwiched in between zones of complete block at smaller or longer cycle lengths. During ventricular stimulation no retrograde V-A conduction could be observed. The findings support the thesis of at least two functionally different A-V pathways in patients with pre-excitation syndrome.     

One to one atrioventricular conduction during atrial pacing at rates of 300/minute in absence of wolff-parkinson-white syndrome

One to one atrioventricular (A-V) or atrio-His bundle (A-H) conduction occurred during right atrial pacing at rates of 300/min in two patients with short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias. Patient 1 had episodes of reciprocating A-V tachycardia and of atrial fibrillation with very fast rates (270 to 290/min) that were slowed to 100 to 135/min after administration of intravenous verapamil. Enhanced A-V (A-H) conduction was exposed only during stimulation from the high right atrium, but not from the low lateral right atrium or coronary sinus. Patient 2 had episodes of atrial flutter with 1:1 A-V conduction and rates of 290/min. The H-V interval was short (25 ms) during sinus rhythm and atrial pacing presumably because conduction occurred through an atrio-“distal” His bundle (atriofascicular) tract. In contrast, the H-V interval was normal (40 ms) in echo beats or when the “proximal” His bundle was stimulated.In these two patients, having as “common denominators” short P-R (and A-H) intervals, narrow QRS complexes and recurrent supraventricular tachyarrhythmias, enhanced A-V (A-H) conduction was (1) possibly due to different electrogenetic mechanisms; (2) pacing-site dependent; (3) manifested, during atrial fibrillation and atrial flutter, by extremely fast ventricular rates; and (4) unrelated to the rate of reciprocating A-V tachycardias because the latter was predominantly a function of anterograde conduction through the “slow” nodal pathway.     

Phenomenon of a complete interventricular (interatrial) block

In 21 cases of separate cardiac cavity excitation (20 of separate ventricular excitation (SVE) and one of separate atrial excitation), 40 right and left QRS complexes were obtained by routine, prolonged and synchronous ECG recording in various standard leads. A differential diagnosis was made between fusion QRS complexes and right and left QRS complexes. Three criteria of fusion ventricular complexes were found to be undiagnostic for right and left ventricular complexes in SVE. SVE has its own electrocardiographic criteria: (1) heterodirectional P waves or QRS complexes separated and unseparated from each other by an isoelectrical interval of less than 0.15 or less than 0.25 s, respectively; (2) in SVE, P-R interval may be no more than 0.06 s shorter than sinus P-R interval; (3) the end vector may be different from or similar to the sinus one. The basis for separate cardiac cavity excitation is functional longitudinal interatrial or interventricular blockade.     

Ventricular pre-excitation revealed by idioventricular rhythm and large QRS tachycardias. Apropos of an operated case

A 15 year old boy presented with palpitations of sudden onset and termination over a two month period. The heart was clinically and radiologically normal. The electrocardiogramme showed sinus rhythm with a short PR interval (0,11 sec) and narrow QRS complexes (0,08 sec) associated with an intermittent escape accelerated idioventricular rhythm (AIVR). During an attack of palpitations a regular tachycardia (250/min) with wide QRS complexes of the same configuration as those of the AIVR (left side delay). The diagnosis of ventricular tachycardia was retained. Endocavitary electrophysiological recording demonstrated preexcitation of the right ventricle associated with accelerated nodal conduction explaining the narrow QRS complexes in sinus rhythm. The wide complex tachycardias initiated and terminated by paired ventricular stimulation were identical to the spontaneous attacks and were attributed to an antidromic reciprocating rhythm. The hypothesis of a rhythm arising from the accessory pathway is suggested. This would explain the identical configuration of the QRS complexes of the AIVR and of the antidromic reciprocating-rhythm and the disappearance of the AIVR after surgical section of the accessory pathway.     

Mahaim and James fibers as a basis for a unique variety of ventricular preexcitation

This report concerns pathologic findings in a 54 year old woman with intermittent preexcitation who died of carcinoma of the breast. Electrocardiograms revealed predominantly normal sinus rhythm with a normal P-R interval and narrow QRS complex. Episodes of sinus rhythm, short P-R interval and QRS widening (with delta wave) were also recorded. During preexcitation QS complexes were noted in leads II, III, aVF, V₁ and V₄ to V₆. Delta waves were negative in leads II, III, aVF and V₁, isoelectric in leads V₄ to V₆ and positive only in leads I, aVL, V₂ and V₃. This case thus defies classification into any known variety of preexcitation.

Complete serial sections, cut through the entire conduction system and both atrioventricular (A-V) rims, totaled 18,600 sections. These revealed no bundle of Kent. Instead, Mahaim fibers histologically identified as His bundle tissue gave off from the A-V bundle to both the right and the left sides of the septum associated with the normal fibers of James. This case reveals that (1) fibers of James can bypass the A-V node, (2) fibers of Mahaim can conduct, and (3) there are types of preexcitation in addition to types A and B.