Improved intraventricular conduction of premature beats after diphenylhydantoin

To determine the effect of diphenylhydantoin on intraventricular conduction in man, we utilized His bundle recordings and coupled atrial pacing to record the relative refractory period of the His-Purkinje system and the functional refractory period of the atrioventricular (A-V) node in 14 patients before and after administration of diphenylhydantoin at a rate of 50 mg/min. Before infusion of diphenylhydantoin (5 mg/kg at a rate of 50 mg/min) His-Purkinje conduction delay occurred with right bundle branch block in nine patients and with left bundle branch block in five patients. After infusion of diphenylhydantoin the onset or degree of His-Purkinje delay was altered in all patients. In nine patients diphenylhydantoin reduced the relative refractory period of the His-Purkinje system to a value less than that of the functional refractory period of the A-V node so that His-Purkinje conduction delay could not be demonstrated after diphenylhydantoin. In five patients, diphenylhydantoin reduced the relative refractory period of the His-Purkinje system or altered the degree of aberrant conduction, or both. Diphenylhydantoin reduced the minimal H₁–H₂ interval achieved before the onset of His-Purkinje block from 421 ± 27 (standard deviation) to 384 ± 34 msec (P <0.01). The functional refractory period of the A-V node was decreased from a control value of 389 ± 39 to 374 ± 26 msec after administration of diphenylhydantoin, but the effect was not statistically significant (P > 0.1). These results establish that diphenylhydantoin has a significant effect on intraventricular conduction in man.     

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.     

Mechanism of the repetitive ventricular response in man

The electrophysiologic characteristics of the repetitive ventricular response that followed an electrically induced single premature ventricular complex were evaluated to determine its mechanism during atrial pacing or sinus rhythm in 30 patients. Seven patients had preexisting bundle branch block. His bundle or right bundle branch deflections did not precede the repetitive complex in 29 of the 30 patients, which implies that the proximal His-Purkinje system was not involved in the reentry circuit. In 24 of 30 patients the QRS axis of the repetitive complex was divergent 45 ° or more from the stimulated complex. In 22 of 30 patients the repetitive complex had a right bundle branch block configuration. In 14 of 18 patients with two or more repetitive complexes, the QRS pattern changed from beat to beat, which implies that either the reentry pathway or conduction was changing. Thus, the repetitive ventricular response, which can be associated with clinically important ventricular arrhythmias, probably represents intraventricular rather than proximal His-Purkinje system reentry.     

Electrophysiologic properties and antiarrhythmic mechanisms of intravenous N-acetylprocainamide in patients with ventricular dysrhythmias

To define electrophysiologic properties and antiarrhythmic mechanisms of N-acetylprocainamide (NAPA), we studied 16 patients with symptomatic ventricular dysrhythmias. Electrophysiologic studies were performed before and after intravenous infusion of NAPA at 20 mg/kg over 20 minutes, achieving plasma concentrations of 24 +/- 3.2 to 35.5 +/- 4.5 micrograms/ml. NAPA did not significantly change sinus cycle length or atrioventricular (AV) conduction times (PA, AH, HV, and QRS), but it lengthened the QTc interval (p less than 0.001) during sinus rhythm. Programmed atrial stimulation revealed that NAPA had no discernible effects on AV nodal conduction; however, it exerted depressive effects on the His-Purkinje system in 9 of 16 patients. In 7 of 16 patients who manifested frequent ventricular premature beats (VPBs), NAPA abolished VPBs in only three of them; NAPA induced progressive prolongation of the premature coupling interval before complete abolition of VPBs. In 8 of 16 patients who had inducible repetitive ventricular response (RVR) because of reentry within the His-Purkinje system, NAPA narrowed or abolished the RVR zone in 3 patients and slowed the RVR rate with widening of the RVR zone in the remaining 5 patients. In 2 of 16 patients with slow ventricular tachycardia (VT), NAPA had no antiarrhythmic effects. By contrast, in the other 2 of 16 patients in whom sustained VT could be reproducibly elicited with programmed ventricular stimulation, NAPA slowed the rate of VT and suppressed VT inducibility. We conclude that electrophysiologic properties of NAPA are slightly different from those of procainamide and that NAPA is not uniformly effective for suppressing ventricular dysrhythmias, but its antiarrhythmic mechanisms are similar to those of procainamide.     

Gap phenomenon in “the right and left bundle branch systems” during retrograde conduction in man

Gap phenomenon in right and left bundle branch systems during retrograde conduction is described in two patients with manifest reentry within the His-Purkinje System (V₃ phenomenon). In this form of gap the premature impulse (S₂) initially blocked in the right bundle branch system and conducted retrogradely via the left bundle branch system as manifested by sudden prolongation of S₂H₂ interval and appearance of V₃. At close coupling intervals S₂ impulse encountered retrograde block in the left bundle branch system and resumed retrograde conduction via the right bundle branch system with S₂H₂ intervals shorter than critical value and was not followed by V₃. However, on further shortening the S₁S₂ intervals S₂ impulse blocked again in right bundle branch system and resumed conduction via the left bundle branch system with S₂H₂ intervals longer than critical values and V₃ reappeared. The mechanism of these gaps is not clear but we believe is similar to the one proposed in Types I and II gaps in antegrade bundle branch conduction and involves proximal delay allowing distal recovery. The similarities and differences between the gap phenomenon in bundle branches during antegrade and retrograde conduction are discussed.     

Effects of digitalis on ventricular myocardial and His-Purkinje refractoriness and reentry in man

The effects of digitalis on retrograde conduction and refractoriness of the His-Purkinje system, ventricular myocardium and reentry within the His-Purkinje system were studied in 17 patients using the ventricular extrastimulus (V₂) technique. Studies were performed, before and 30 minutes after intravenous administration of ouabain, 0.01 mg/kg. After treatment with ouabain, there was a significant decrease in the functional refractory period (266 ± 19 to 254 ± 18 msec, P < 0.001), relative refractory period (253 ± 17 to 240 ± 16 msec, P < 0.001) and effective refractory period (242 ± 23 to 231 ± 24 msec, P < 0.005) of the ventricular muscle. In contrast, there was no significant change in retrograde His-Purkinje conduction and refractoriness. The phenomenon of reentry within the His-Purkinje system characterized by the reentrant beat (V₃) at critical retrograde conduction delays in the His-Purkinje system (V₂-H₂) within a narrow range of V₁–V₂ intervals was seen in 10 of 17 patients. Ouabain increased and shifted to the left the zone of reentry within the His-Purkinje system in 7 of 10 patients (36 ± 23 to 55 ± 23 msec, P < 0.001) and decreased it by 10 to 30 msec in the remaining 3 patients. The critical V₂-H₂ (186 ± 29 to 193 ± 27 msec, difference not significant [NS]) and V₁–V₂ (299 ± 30 to 294 ± 36 msec, NS) intervals for reentry did not significantly change after ouabain. However, the minimal V₁–V₂ intervals (266 ± 26 to 253 ± 25 msec, P < 0.025) decreased significantly, whereas the maximal V₂-H₂ intervals (266 ± 40 to 239 ± 37 msec, P < 0.01) increased significantly.

Thus, in the intact human heart, digitalis (1) significantly decreased all measures of ventricular myocardial refractoriness, (2) had no significant effect on retrograde conduction and refractoriness of the His-Purkinje system, and (3) widened the zone of reentry within the His-Purkinje system due to shortening of the functional refractory period of the ventricular muscle with attainment of longer V₂-H₂ delays.     

Effects of digoxin on atrioventricular conduction patterns in man

Digoxin was acutely administered to 17 patients, and its effects on atrioventricular (A-V) conduction were assessed. In the control state, before administration of digoxin, progressively premature atrial depolarization showed conduction delay and block confined solely to the A-V node in eight patients and to both the A-V node and the more distal His-Purkinje tissue in nine patients. His-Purkinje conduction delay was manifested on the surface electrocardiogram by ventricular aberration. After administration of digoxin, an early atrial premature impulse either was blocked in the A-V node or reached the distal intraventricular conduction system so late that block or conduction delay below the His bundle was reduced or no longer occurred. Ventricular aberration on the surface electrocardiogram was thus reduced or eliminated. These effects of digoxin on A-V conduction were due to its effect on the A-V node of slowing conduction of a premature impulse. Such action on the A-V node may abolish aberrant ventricular conduction in atrial fibrillation.     

Effects of intravenous amiodarone in patients with inducible repetitive ventricular responses and ventricular tachycardia

We studied the effects of intravenous amiodarone administration (5 mg/kg) on reproducible repetitive ventricular responses and ventricular tachycardia (VT) induced by programmed electrical stimulation of the heart in 32 patients. Intravenous amiodarone prevented induction of bundle branch reentry in only 2 of 11 patients (18.2%) and did not change His-Purkinje conduction and refractoriness in the remaining 9 of 11 (81.8%) patients. In contrast to the small effect of intravenous amiodarone on bundle branch reentry, the drug completely abolished intraventricular reentry in three of nine (33.3%) patients and in the remaining six of nine (66.7%) patients decreased the number of intraventricular reentrant beats from up to five beats in control to one to two beats after the drug. The drug also prevented induction of VT (greater than or equal to 5 ventricular ectopic beats in a row) in three of five (60%) patients with nonsustained VT and in three of seven (42.9%) patients with sustained VT. In two of seven (28.6%) patients with sustained VT, only nonsustained tachycardia could be induced after drug administration. In another two of seven (28.6%) patients, sustained VT with slower rates was induced after the drug. In 11 of 12 (91.7%) patients with VT the coupling interval between the last stimulus and the first ventricular beat increased after drug administration. These effects of intravenous amiodarone occurred in the absence of effect on ventricular effective refractory period. These findings suggest that intravenous amiodarone might have greater effect on diseased ventricular tissue, the site of reentry in VT, than on healthy ventricular tissue.     

Atrioventricular node reentry: Intravenous verapamil as a method of defining multiple electrophysiologic types

Fourteen patients with recurrent supraventricular tachycardia (SVT) underwent electrophysiological evaluation. Each patient was shown to have reentry confined to the region of the atrioventricular (AV) node. Verapamil, 0.075 to 0.15 mg/kg was administered intravenously to each patient during a stable episode of SVT, resulting in termination in each instance. There was more than one mechanism for termination of SVT. Nine patients showed termination by anterograde AV node block preceded by an increase in conduction time in the anterograde limb of the tachycardia circuit (Ae-H intervals) with no change in the conduction time in the retrograde limb (H-Ae intervals). Three patients showed termination by block in the retrograde limb of the circuit preceded by increases in both Ae-H and H-Ae intervals. An additional example of termination by spontaneous ventricular premature complexes and usurpation by sinus rhythm were also seen. Common features were that verapamil had significant effects on anterograde and retrograde conduction and refractoriness in the AV node. It prolonged the refractory periods of both fast and slow pathways in patients with dual anterograde AV node pathways, and observable effects on retrograde conduction and refractoriness were seen even in patients with constant ventriculoatrial conduction times during incremental ventricular pacing in a control study. However, three distinct groups of patients were identified on the basis of their response to ventricular pacing in a control study and upon verapamil effects recorded during their SVT. An explanation for these latter findings may be that there is a normal variation in the retrograde response of parts of the AV node to ventricular pacing, and a variability in some of the patients' responses to verapamil.     

Prognostic significance of repetitive ventricular response during programmed ventricular stimulation

To determine the incidence and prognostic significance of the repetitive ventricular response, a retrospective study was performed in 65 patients (49 male, 16 female, mean age ± standard deviation 55 ± 11 years) with coronary artery or myocardial disease and a variety of cardiac rhythm disorders. Programmed right ventricular stimulation was performed at a basic pacing rate of 120 beats/min using one (S₂) and two (S₂-S₃) premature stimuli. The data were analyzed as to the presence or absence of a repetitive ventricular response and the patients' outcome ([1] sudden death at 1 hour or less or documented ventricular fibrillation without myocardial infarction; [2] survival or death from noncardiac causes or nonsudden death).A repetitive ventricular response was observed in 23 (35.4 percent) of 65 patients after one and in 31 (48.4 percent) of 64 patients after two premature stimuli. It occurred in 9 of 9 patients with ventricular fibrillation and in 14 (82.4 percent) of 17 patients with ventricular tachycardia. The mean follow-up period was 76 ± 39 weeks. Sixteen patients were classified as dying suddenly; the remaining patients were considered surviving (or dying nonsuddenly). After one premature stimulus, a repetitive ventricular response was observed in 32.7 percent of patients surviving or with nonsudden death and in 43.8 percent of patients with sudden death or malignant ventricular arrhythmias. After two premature stimuli, the incidence of a repetitive ventricular response increased from 40.8 percent in patients surviving or with nonsudden death to 68.8 percent in patients with sudden death; 6 (12.2 percent) of 49 patients surviving or with non-sudden death and 9 (56.3 percent) of 16 patients with sudden death had more than three ventricular echo beats. All nonsurviving patients who demonstrated a repetitive ventricular response had intraventricular reentry. Depending on the rigidity of the criteria used (that is, the number of echo beats), the sensitivity of the test ranged between 37 and 88 percent and specificity ranged between 45 and 92 percent. The proportion of false positive results was high (33 to 66 percent); but the proportion of false negative results was low (8 to 18 percent).This retrospective study showed a correlation between sudden death and the incidence and number of repetitive ventricular responses (depending on the number of premature stimuli) and the type of reentrant beats (bundle branch reentry or intraventricular reentry).     

Gap in A-V conduction in man; types I and II

The mechanism of the “gap” phenomenon in A-V conduction was studied in man during premature atrial stimulation studies using His bundle recordings. Previous reports have demonstrated that while relatively late premature atrial impulses are blocked within the His-Purkinje system, earlier premature atrial impulses may successfully propagate to the ventricle if they encounter sufficient A-V nodal delay to allow recovery of the distal area of refractoriness (Type I “gap”). In the present report, an analogous mechanism of the “gap” is described which is due to delay within the His-Purkinje system (Type II “gap”). Relatively late premature atrial impulses were noted to block within the His-Purkinje system, similar to the findings in Type I. Conduction resumed in Type II, however, when earlier premature atrial impulses encountered delay in a relatively proximal area of the His-Purkinje system, allowing more complete recovery of the distal area of refractoriness. Both types of gap phenomena represent examples of apparent supernormal conduction.     

Initiation of ventricular tachycardia by reentry within the bundle branches: Implications for electrophysiologic testing of antiarrhythmic drugs

A nonpaced third ventricular depolarization (V₃) often occurs when, during ventricular pacing, single ventricular extrastimuli produce critical retrograde His-Purkinje conduction delay. V₃ has been attributed to macroreentry within the bundle branches. However, the relation of bundle branch reentry to other ventricular arrhythmias has been uncertain. In the three patients presented in this report, macroreentry over a bundle branch reentrant circuit consistently initiated ventricular tachycardia that utilized a different, probably microreentrant, circuit. In two of the three patients, ventricular tachycardia was induced by a second ventricular extrastimulus delivered just before the macroreentrant V₃ would have been expected, as well as by macroreentrant V₃ depolarizations resulting from single extrastimuli. This suggests that ventricular tachycardia induction depended not on bundle branch reentry itself, but on the occurrence of a closely coupled third ventricular complex, whether paced or reentrant.When, during single ventricular extrastimulus testing, ventricular tachycardia follows bundle branch macroreentry, modification or abolition of the bundle branch reentry by an antiarrhythmic drug may impair evaluation of the drug's effect on the ventricular tachycardia microreentry. This mechanism of ventricular tachycardia induction should be recognized in order to avoid selection of possible inappropriate antiarrhythmic therapy.     

Asymmetry of retrograde conduction and reentry within the His-Purkinje system: A comparative analysis of left and right ventricular stimulation

Objectives. The purpose of this study was to delineate retrograde His-Purkinje system conduction and reentry (V₃phenomenon) during left ventricular extrastimulation and compare them with right ventricular extrastimulation.Background. The V₃phenomenon has been well described in the past during right ventricular extrastimulation; however, it has not been studied systematically during left ventricular extrastimulation.Methods. Left and right ventricular pacing were performed in 13 patients. Retrograde and anterograde routes of impulse propagation were determined on the basis of the sequence of His (H) and right bundle (RB) potentials, H-RB intervals, as well as the QRS configuration and axis of V₃beats.Results. During right ventricular pacing, retrograde conduction of V₂, when discernible, occurred exclusively through the left bundle at all coupling intervals equal to or shorter than the His-Purkinje relative refractory period, with the exception of two isolated beats. During left ventricular extrastimulation, His bundle activation was through the left bundle in nine patients and through the right or left bundle in three other patients. In one patient, the route could not be determined. The V₃phenomena occurred in eight patients during right ventricular pacing. Seven patients had a left bundle branch block pattern QRS configuration, and one had a right bundle branch block pattern configuration. V₃beats occurred in five patients during left ventricular apex pacing: left bundle branch block pattern configuration in one patient and right bundle branch block pattern configuration in four. In three of these four patients, the reentry was interfascicular and limited to the left bundle branch system.Conclusions. The left-sided His-Purkinje system is the preferred retrograde route of impulse propagation during both left and right ventricular extrastimulation. Reentry within the His-Purkinje system elicited by right ventricular extrastimulation involves both bundle branches, whereas this reentry tends to occur within the left-sided His-Purkinje system during left ventricular pacing.     

Electrophysiologic mapping to determine the mechanism of experimental ventricular tachycardia initiated by premature impulses: Experimental approach and initial results demonstrating reentrant excitation

Epicardial activation patterns were determined during repetitive responses and nonsustained and sustained ventricular tachycardias induced by premature impulses in infarcted canine hearts. A multiplexing system enabled recordings to be obtained from up to 192 electrodes simultaneously either from the entire epicardial surface with a sock electrode array or only from the sheet of epicardial muscle that survives over the infarcts, with a plaque electrode array. In hearts with an infarct caused by permanent occlusion of the left anterior descending coronary artery, the earliest epicardial excitation during nonsustained tachycardias occurred on the anterior left ventricle at the border of the infarcted region and in epicardial muscle surviving over the infarcted region. Circuituous conduction patterns leading to reentry occurred in the epicardial muscle over the infarct and probably caused the arrhythmias. During sustained tachycardia in hearts with an infarct caused either by permanent or temporary occlusion of the left anterior descending coronary artery, the earliest epicardial excitation also occurred at the border of the infarcted region, but there was no evidence of reentry in the surviving epicardial muscle.     

Comparison of the electrophysiologic effects of intravenous and oral verapamil in patients with paroxysmal supraventricular tachycardia

The electrophysiologic effects of intravenous verapamil (a bolus dose of 0.15 mg/kg body weight followed by infusion of 0.005 mg/kg per min) were compared with those of oral verapamil (80 mg every 6 hours for 48 hours) in eight patients who had paroxysmal Supraventricular tachycardia. The mechanism of tachycardia was atrioventricular (A-V) nodal reentry in four patients and A-V reentry utilizing an accessory pathway for retrograde conduction in the remaining four. The electrophysiologic effects of oral and intravenous verapamil were similar. Both preparations significantly prolonged anterograde effective and functional refractory periods of the A-V node (p < 0.001). Both significantly increased the shortest pacing cycle length maintaining 1:1 anterograde conduction over the A-V node (p < 0.001). Retrograde conduction over the A-V node was greatly prolonged with verapamil in one patient but was unaffected in the others. There was no significant effect on sinoatrial conduction time, sinus nodal recovery time or atrial or ventricular refractoriness. Both preparations prevented induction of tachycardia in six patients none of whom had recurrence of sustained tachycardia while receiving long-term oral therapy (5 to 10 months). Neither preparation had a significant effect in two patients and this predicted failure of long-term oral therapy in one of these patients.The results of acute drug testing with intravenous verapamil can be extrapolated to predict the electrophysiologic results and response to long-term therapy with oral verapamil.     

Bundle-Branch Reentrant Ventricular Tachycardia: A Possible Mechanism of Flecainide Proarrhythmic Effect

A 42-year-old male with cardiomyopathy and paroxysmal at atrial fibrillation was on chronic oral amiodarone therapy (200 mg/day) and received an additional 400 mg of flecainide per day because his nondocumented palpitations recurred. Ten syncopes occurred in the two following months and the patient was referred for electrophysiologic study. The basic H#V interval was prolonged (80 msec) and QRS slightly prolonged (110 msec). Programmed ventricular stimulation consistently found a critical SH delay (260 msec) that was followed by a left bundle-branch block type of QRS. The latter was always preceded by a His deflection (H), thereby evoking His-Purkinje reentry. Three premature beats induced a rapid (cycle length 270 msec), sustained, poorly tolerated ventricular tachycardia (VT) with a QRS morphology identical to the bundle-branch reentrant phenomenon.
Each ventricular electrogram was preceded by an H, H-V varying from 100 to 130 msec. Three weeks after flecainide withdrawal, the H-V interval was 60 msec and no VT was inducible. This observation is representative of a proarrhythmic effect of flecainide in association with amiodarone.
Bundle-branch reentry ventricular tachycardia is the most likely mechanism of arrhythmia-aggravation in this observation. It could have been induced because of intraventricular depression of conduction.     

Initiation of two distinct forms of atrioventricular nodal reentrant tachycardia during programmed ventricular stimulation in man

Of 42 patients with supraventricular tachycardia related to dual atrioventricular (A-V) nodal pathway conduction, 8 had sustained tachycardia induced during programmed ventricular stimulation. The characteristics of the tachycardia in three patients suggested that the A-V nodal reentrant tachycardia used a slow pathway for anterograde conduction and a fast pathway for retrograde conduction (slow-fast form). In these patients, the retrograde effective refractory period was longer in the slow than in the fast pathway. Ventriculoatrial (V-A) conduction curves (V₁-V₂, A₁-A₂) were smooth. Ventricular premature beats, being conducted retrograde over the fast pathway, could activate the slow pathway in an anterograde direction, initiating the slow-fast form of A-V nodal reentrant tachycardia. In the remaining five patients, the tachycardia used a fast pathway for anterograde conduction and a slow pathway for retrograde conduction (fast-slow form). In these patients, the retrograde effective refractory period was longer in the fast than in the slow pathway. V-A conduction curves (V₁-V₂, A₁-A₂) could be either smooth or discontinuous if there was a sudden increase in V-A conduction time. Ventricular premature beats, conducted retrograde over the slow pathway, could activate the fast pathway in an anterograde direction, establishing a tachycardia circuit in reverse of the slow-fast form. In both groups of patients, the ventricular pacing cycle length appeared to be a crucial factor in the ability to expose functional discordance between the two A-V nodal pathways during retrograde conduction.The fast-slow form of A-V nodal reentrant tachycardia, similar to the slow-fast form, could also be induced during atrial premature stimulation in two patients. In this situation, the slow pathway having an anterograde effective refractory period longer, than that of the fast pathway was a requisite condition; anterograde A-V nodal conduction curves (A₁-A₂, H₁-H₂) were smooth. Atrial premature beats, conducted anterograde over the fast pathway, could activate the slow pathway in a retrograde direction resulting In an atrial echo or sustained fast-slow form of A-V nodal reentrant tachycardia.     

Gap, phase III and IV block and supernormal conduction of the right bundle branch

A recent review of the literature corroborated that several factors explained why supraventricular impulses falling gradually earlier in the cycle could traverse the His-Purkinje system while other impulses occurring later could fail to do so. The present report deals with the coexistence (in the same patient) of three distinct mechanisms whereby progressively more premature impulses could be "unexpectedly" conducted. Phase III left bundle branch block coexisted with the following conduction disturbances in the right bundle branch; late "pseudosupernormal" conduction sandwiched in between periods of phase III and phase IV block; intermediate "pseudosupernormal" conduction resulting from the so-called type 2 gap, during which propagation occurred, but with H-V intervals longer than later in the cycle; early "true" supernormal conduction (related temporarily to the end of the T wave) exposed when a premature ventricular beat reached the affected zone in a concealed retrograde fashion. These findings show how, with block late in the cycle, conduction in earlier part of the cycle was not always due to "true" supernormal conduction.     

Observations on the mechanism of one type of so-called supernormal A-V conduction

The mechanism of one type of so-called supernormal A-V conduction was elucidated in 11 subjects during premature atrial stimulation studies using His bundle electrogram recordings. At relatively long R-P intervals atrial impulses failed to conduct to the ventricles and were blocked distal to the bundle of His. At shorter R-P intervals A-V conduction resumed. The more premature atrial impulses encountered greater A-V nodal delay (longer A-H interval) and arrived within the His-Purkinje system after the latter was more completely repolarized. The electrophysiological mechanism for this type of so-called supernormal A-V conduction is based on the relationship between the state of refractoriness of the A-V nodal and His-Purkinje conduction systems.