Reinier M. Schuilenburg

Electrical Stimulation of the Heart in Patients with Ventricular Tachycardia

The initiation and termination of tachycardias were studied in five patients who suffered from recurrent attacks of ventricular tachycardia. In four, coronary artery disease with old myocardial infarction was present. A ventricular tachycardia could be initiated in all patients by a single right ventricular premature beat given during regular driving of the right ventricle. The tachycardia could be terminated by a single right ventricular premature beat, or two right ventricular premature beats given in close succession. In four of our patients an early right ventricular premature beat was followed by the next QRS complex of the tachycardia after an interval shorter than compensatory. Our results favor reentry as the causal mechanism for the tachycardias in our patients. Possible pathways for circus reentry leading to ventricular tachycardia can theoretically be composed of (1) the bundle branches, (2) Purkinje fibers with or without adjacent ventricular myocardium, (3) infarcted or fibrotic ventricular tissue, and (4) combinations of (1), (2), and (3).

The Role of Premature Beats in the Initiation and the Termination of Supraventricular Tachycardia in the Wolff-Parkinson-White Syndrome

In four patients with WPW syndrome atrial and ventricular premature beats were induced and the changes in form of the ventricular and atrial complexes were studied. Results indicate that, depending upon the timing of the premature atrial beat and the state of refractoriness of the His and Kent bundles, excitation of the ventricles occurs predominantly through the atrioventricular nodal system, predominantly through the Kent bundle or exclusively through one or both conduction systems. With short delays conduction through the Kent bundle may be blocked and only normal excitation of the ventricles occurs. In one patient with a history of attacks of tachycardia these normal QRS complexes were followed by retrograde activation of the atria by the Kent bundle, and attacks of supraventricular tachycardia of shorter or larger duration occurred. They stopped spontaneously, sometimes by delay or block, either of retrograde Kent conduction or of antegrade A-V nodal conduction, making it possible for the sinus node to capture the ventricles. They also could be terminated by induced atrial premature beats.In two patients tachycardias could be induced by appropriately timed ventricular premature beats during regular driving of the right ventricle. In one of these patients a circus movement, involving the Kent bundle, is probably present. By appropriate stimulation of the atria or ventricles during an attack of supraventricular tachycardia in this patient, one cycle length could be shortened without changing those of the following beats. These results suggest that a circus movement involving the atria, the normal atrioventricular conduction system and the Kent bundle is present. In the other patient, not fulfilling the WPW criteria, ventricular or atrial premature beats did not interfere with the basic rhythm of the tachycardia. Two hypotheses for this tachycardia are given: nodal tachycardia caused by rapid firing of the A-V node or a nodal tachycardia caused by a reciprocal mechanism in the A-V junction. The attacks could be blocked too by appropriately timed atrial and ventricular premature beats. No ventricular type of tachycardia could be demonstrated.

Early identification of patients developing late in-hospital ventricular fibrillation after discharge from the coronary care unit

Abstract In an initial retrospective study, covering 3 years, 30 (3 percent) of 966 patients consecutively discharged from the coronary care unit, were found to have sustained late in-hospital ventricular fibrillation 10 to 38 days after myocardial infarction. Of these 30 patients, 18 (60 percent) died in the hospital and 14 (47 percent) had anteroseptal infarction complicated by right or left bundle branch block. In a later prospective study, covering 2 1 2 years, 47 consecutive coronary care unit survivors with anteroseptal infarction complicated by right or left bundle branch block were kept in the monitoring area for 6 weeks after infarction. Seventeen of these 47 (36 percent) sustained late in-hospital ventricular fibrillation. Neither the type nor the duration of bundle branch block affected the Incidence of late in-hospital ventricular fibrillation. Six (35 percent) of the 17 patients with ventricular fibrillation died in the hospital. Three died from ventricular fibrillation, and of six patients treated with infarctectomy, another three died postoperatively. Of 11 hospital survivors with late in-hospital ventricular fibrillation, followed up for 1 to 30 months, 1 died suddenly within 1 month. Of the remaining 884 patients who were not kept in the monitoring area after coronary care unit discharge, 8 (0.9 percent) sustained late ventricular fibrillation (with 3 in-hospital deaths) and 4 (0.5 percent) others died suddenly in hospital. The results indicate that coronary care unit survivors with anteroseptal infarction complicated by right or left bundle branch block should be kept in the monitoring area for 6 weeks.

Factors Influencing Prognosis of Bundle Branch Block Complicating Acute Antero-Septal Infarction The Value of His Bundle Recordings

Of 50 consecutive patients with bundle branch block (BBB) complicating acute antero-septal infarction, 37 died in hospital. Patients with BBB of delayed onset or BBB of short duration had a significantly lower mortality. His bundle recordings were made in 35 patients without pulmonary edema or shock at the time of appearance of BBB. Thirteen of 16 patients with prolonged H-V intervals died compared to nine of 19 with normal H-V intervals (P < 0.05). In patients with bifascicular block, 11 of 15 with prolonged H-V intervals developed complete A-V block compared to one of ten with normal H-V intervals (P < 0.005).Twenty-five of 33 patients with normal P-R intervals died compared to eight of 12 with first degree A-V block. Seven of 15 patients with prolonged H-V intervals had normal P-R intervals and four of these seven developed complete A-V block. We conclude that the length of P-R interval has no prognostic significance and is of limited value in predicting both prolonged H-V interval and development of complete A-V block. In contrast, His bundle recordings are of value in identifying patients with BBB complicating antero-septal infarction who are at immediate high risk for development of complete A-V block and death.

Conduction Disturbances Located within the His Bundle

Four patients are described with different degrees of conduction disturbance within the His bundle. In one patient with a Mobitz type II atrioventricular (A-V) block with normal QRS complexes the blocked atrial beats were followed by a His potential. Since the QRS complexes of the conducted beats were completely normal, the site of the block was thought to be in the distal part of the His bundle. In the other three patients with a 2:1 A-V block, a nearly complete A-V block, and a complete A-V block, two distinct His potentials could be discerned, one (H) following each atrial beat, the other (H′) preceding each ventricular activation. In the patient with 2:1 A-V block a Wenckebach phenomenon within the His bundle could be produced at certain atrial driving rates. Impulse conduction through the A-V node was normal in all four cases, as could be concluded from the effect of increased atrial driving rate and of accurately timed atrial premature beats. The site of the block could not be predicted from the conventional electrocardiogram.

Ventricular Echo Beats in the Human Heart Elicited by Induced Ventricular Premature Beats

In three patients, all having as their only hemodynamic abnormality an elevated cardiac index at rest, ventricular echo beats could be elicited by ventricular premature beats induced during regular driving of the ventricle. The occurrence of ventricular echo beats was in each case limited to a small delay-range of the premature beat. Retardation of retrograde conduction of the premature ventricular impulse to the atria appeared to be a necessary condition for the initiation of the echo phenomenon.One of the patients had retardation of antegrade A-V conduction of sinus and premature atrial beats. Atrial echo beats could be elicited in this case.The genesis of the ventricular echo phenomenon in these cases could be explained by the dual conducting system theory.

Observations on atrioventricular conduction in patients with bilateral bundle-branch block.

Atrioventricular conduction was studied in three patients, each representing a different grade of bilateral bundle-branch block. His bundle activity was recorded by a catheter technic. Two of the three patients had experienced Adams-Stokes attacks.The first patient had right bundle-branch block with left axis deviation at the time of catheterization. Increases in the atrial driving rate resulted in progressive lengthening of the A-H interval, the H-V interval remaining constant and within normal limits. Second degree A-V block occurred at atrial rates higher than 140/min. The site of this block was located above the His bundle. On no occasion was the impulse blocked distally to the His bundle.The second patient had a Mobitz type II A-V block with complete left bundle-branch block and a prolonged P-R interval in the conducted beats. The block of the nonconducted beats could be located distal to the His bundle. H-V block occurred more frequently when the atrial rate was increased. Second degree A-H block occurred at rates above 140/min. At these rates interesting patterns were seen due to conduction impairment at two levels in the A-V conduction system.The third patient presented with complete A-V block. The site of this block could be located at a level lower than the His bundle. A-H conduction studied with increases of atrial rate and with atrial premature beats seemed to be normal. There was evidence for the existence of retrograde V-A conduction in this patient.

Rate-Dependency of Functional Block in the Human His Bundle and Bundle Branch-Purkinje System

In eleven patients in whom atrial premature stimulation elicited functional block in the conduction system distal to the atrioventricular (A-V) node, the influence of atrial driving rate was studied. Functional conduction disturbances in the left bundle branch-Purkinje system were produced by driving the atria at a rate just above the spontaneous sinus rate and by introducing premature atrial stimuli. In five patients this was associated with block or delay of conduction in the right bundle branch-Purkinje system and in one with block within the His bundle. In these patients it was shown that the ultimate QRS configuration of the premature beat was determined by different conduction delays in the three parts of the bundle branch system. In three patients complete block of impulse conduction could be produced below the level of the His bundle, in one within the His bundle. In these four patients conduction delay of earlier atrial premature beats within the A-V node with resumption of conduction in the more peripheral pathways, gave rise to the phenomenon of the A-V gap. In two patients functional conduction delay in the contralateral bundle branch caused pseudo-normalization of a pre-existent complete right bundle branch block pattern, indicating that this pattern may not be caused by complete block, but by delayed conduction in the right bundle branch.In ten of the eleven patients functional block or delay of atrial premature beats in the peripheral conduction system became less pronounced as the driving rate was increased. In nine of these ten the phenomenon disappeared completely at higher rates; in six this occurred with an increase in rate of only 20 beats/min. The A-V gap phenomenon present in four cases at the lowest rate disappeared at higher rates in all four. It was concluded that functional conduction disturbances in the peripheral conduction system are favored by a low basic heart rate and that this rate dependency is caused by a differential influence of heart rate upon the functional properties of the A-V node and of the more peripheral parts of the conduction system.

Bundle Branch Block and Acute Myocardial Infarction

When bundle branch block (BBB) complicates acute myocardial infarction, the site of infarction is usually anteroseptal (41,306,319,383,604,726). During complete infranodal block the escape pacemaker that emerges from the peripheral Purkinje system (385,667) is unstable and has a slow rate (41,306).

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

Abstract 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.