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.     

Sinus nodal echoes. Clinical case report and canine studies

Sinus nodal echoes are illustrated in (1) a case report, and (2) a study of the effects of atrial premature beats after atrial drive in dogs. When atrial premature beats confront the sinus node while it is still refractory, 3 types of response may be seen: (1) Complete interpolation—the subsequent sinus beat (or escape) comes precisely at the expected time; (2) incomplete interpolation—the subsequent sinus beat is delayed; and (3) sinus echoes—the sinus beat appears earlier than expected. In all 3 instances the node is entered, but the pacemaker fails to be reset. Although the echo has the form of a sinus beat, it is followed by a pause, presumably as a result of repenetration of the sinus node through pathways unused during exit. The curves characterizing the expansion by vagal stimulation of the nodal refractory period and total echo circuit time are defined, together with the latency of cholinergic effect on nodal refractoriness, sinus automaticity and exit conduction of the echo. The secondary concealment zone of a completely interpolated atrial premature beat is established. Atrial preexcitation (before the echo) sometimes evokes a second echo. The limiting factor on sustained sinoatrial reciprocation thus appears to be total echo circuit time rather than refractoriness of atrium or echo entrance pathways. The repetitive echoes seen in this study may be the basis for some clinical cases of sinus or atrial tachycardia.     

Simultaneous anterograde fast-slow atrioventricular nodal pathway conduction after procainamide

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

Atrioventricular alternating Wenckebach periodicity: conduction patterns in multilevel block

Atrioventricular (A-V) conduction patterns were analyzed in three patients with atrial pacing-induced alternating Wenckebach periodicity. These cases were unique because in each (1) separate levels of block responsible for the conduction disturbance were located above and below the His bundle recording site, and (2) there were several departures from the simple alternating Wenckebach pattern. Apparent supernormal conduction, temporary 1:1 conduction and a specific form of gap in A-V conduction resulted from the interplay of many factors including a simple mathematic relation of the blocking ratio at the two levels, the characteristics of the Wenckebach cycles, and the cycle length-dependent features of refractory periods at the different sites. The findings indicate that (1) delay in proximal impulse transmission is usually the critical factor in overcoming prolonged distal refractoriness and producing variable conduction patterns during the course of alternating Wenckebach periodicity; (2) many irregularities in alternating Wenckebach periodicity can be explained by known electrophysiologic mechanisms; and (3) simple mathematic equations alone are too rigid to reflect properly the dynamic process underlying this conduction disturbance.     

Wenckebach periods with repetitive block: evaluation with His bundle recording

Two patients are reported in whom repetitive block of two consecutive P waves occurred during Wenckebach beating induced by atrial pacing. His bundle recordings revealed block proximal to H in the first case, suggesting inhomogeneous conduction in the A-V node. In the second case, long cycle lengths were produced in the His-Purkinje system due to A-V nodal Wenckebach periods. The long cycles prolonged refractory periods in the His Purkinje system so that subsequent beats (short cycles) were blocked distal to H.The repetitive block of consecutive multiple atrial impulses could result in unexpected degrees of ventricular asystole during usually benign Type I second-degree A-V block.     

Atrial conduction: effects of extrastimuli with and without atrial dysrhythmias

The effects of cycle length and stimulation site on intraatrial conduction and refractoriness were evaluated in patients with and without atrial flutter (AFI) or fibrillation (AF) using the extrastimulus technique. Nineteen patients with spontaneous sustained AFI or AF were compared with 19 control patients. Programmed stimulation was performed at the right atrium and coronary sinus at drive cycle lengths of 600 and 450 ms. The atrial effective refractory period was similar in the patients with atrial dysrhythmias and the control group. The right atrial effective refractory period at a drive cycle length of 600 ms was significantly shorter in patients with AF (211 ms) than in patients with AFI (235 ms, p = 0.05). The conduction time of late (coupling intervals more than 50% of the drive cycle length) premature impulses was similar in the patients with atrial dysrhythmias and the control group. However, early extrastimuli (coupling intervals less than 50% of the drive cycle length) at a drive cycle length of 600 ms produced significantly more intraatrial conduction delay in the patients with atrial dysrhythmias than in the control patients. At a drive cycle length of 450 ms, similar delays in intraatrial conduction occurred in the patients with and without atrial dysrhythmias because of an increase in the maximal-observed intraatrial conduction delay in the control patients. This study shows that delay in conduction of early premature atrial stimuli at a drive cycle length of 600 ms is a marker of patients with spontaneous AFI and AF.(ABSTRACT TRUNCATED AT 250 WORDS)     

Maturational changes in ventriculoatrial conduction in the intact canine heart

This study reports on the changes in ventriculoatrial (VA) conduction that occur with maturation. Programmed atrial and ventricular premature extra-stimulation (coupled to a fixed paced cycle length) and rapid atrial pacing were performed in three groups of dogs: Group I = 8 neonates aged 5 to 14 days, Group II = 9 young dogs aged 6 to 9 weeks and Group III = 10 adult dogs. High right atrial, His bundle and right ventricular electrograms were recorded. There were no differences in the AH intervals at rest. In all but five animals, atrioventricular conduction was limited by the atrial functional refractory period (Group I, 109 +/- 12 ms; Group II, 152 +/- 22 ms; Group III, 167 +/- 19 ms). As expected, with rapid atrial pacing, Wenckebach conduction developed at a shorter cycle length in the younger animals (Group I, 145 +/- 20 ms; Group II, 153 +/- 15 ms; Group III, 200 +/- 25 ms, p less than 0.01). Ventriculoatrial conduction was documented in 87% of Group I puppies and 100% of Group II, but only 40% of Group III dogs. The effective and functional refractory periods of the VA conduction system were significantly shorter in the more immature groups of dogs (effective/functional: Group I, 124 +/- 27/168 +/- 22 ms; Group II, 139 +/- 23/202 +/- 13 ms; Group III, 270 +/- 28/326 +/- 25 ms; p less than 0.01). Relative to the adult dog, the immature heart showed a greater incidence of VA conduction and shorter VA refractory periods. This enhanced VA conduction may be of physiologic importance in the initiation and perpetuation of certain supraventricular arrhythmias.     

Pacing techniques in the management of supraventricular tachycardias. Part 2. An implanted atrial synchronous pacemaker with a short atrioventricular delay for the prevention of paroxysmal supraventricular tachycardias.

An implanted atrial synchronous pacemaker with an atrioventricular delay of 30 msec is described. This pacemaker was implanted into a patient with paroxysmal supraventricular tachycardia due to an intra AV nodal reciprocal mechanism. The pacemaker was able to trigger from atrial potentials following atrial premature beats down to a coupling time of 300 msec. Following each triggering atrial potential, a ventricular stimulus was applied 30 msec later thereby producing a ventricular premature beat in response to each sinus beat or each atrial premature beat. Retrograde conduction from this atrial premature beat blocked the re-entry mechanism within the AV node and prevented the initiation of tachycardia. A detailed discussion on all parameters of function of this pacemaker is presented.     

Sinus nodal reentry. Effect of quinidine

The recently developed experimental model for sinus nodal reentry was used to assess the effect of quinidine in 20 dogs. Sinus nodal reentry was demonstrated in 19 dogs and was abolished in all dogs when plasma levels of quinidine (average 4.8 mg/liter) were in the therapeutic range after an average infusion time of 7 minutes. Characteristically in 15 dogs, quinidine increased atrial refractoriness and slowed atrial conduction so that the arrival time of the atrial premature beat (A₂) in the region of the sinus node fell outside the reentry zone and sinus nodal reentry was terminated. Conduction delay along the reentrant pathway preceded loss of sinus nodal reentry in 6 of these 15 dogs, thereby suggesting that quinidine-induced conduction delay and block along the reentrant pathway may be another mechanism for abolishing sinus nodal reentry. In the four remaining dogs in which sinus nodal reentry was abolished when the premature beat continued to fall within the reentry zone, the latter mechanism seems likely.     

Electrophysiologic effects of intravenous metoprolol

We evaluated the electrophysiologic effects of intravenous metoprolol, a selective beta-1-blocking agent, in 12 patients. Electrophysiologic parameters were measured during the control period, immediately following, and 4 to 6 hours after infusion of 0.15 mg/kg. Metoprolol serum concentration was serially measured in 6 of the 12 patients. Immediately after metoprolol infusion, the sinus cycle length increased by 20% from 738 +/- 166 msec to 885 +/- 181 msec (p less than 0.01), AH interval during sinus rhythm increased by 34% from 83 +/- 27 msec to 112 +/- 37 msec (p less than 0.01), and antegrade atrioventricular (AV) nodal Wenckebach cycle length increased by 20% from 360 +/- 188 msec to 432 +/- 199 msec (p less than 0.01). Sinus node recovery time and sinoatrial conduction time did not become abnormally prolonged in any patient. His-Purkinje conduction was unaltered. High atrial and ventricular refractory periods were modestly increased (less than 15 msec); the increase in refractoriness reached statistical significance when repeat measurements were made at 4 to 6 hours. No adverse effects were noted. Metoprolol serum concentration at the time of peak measured electrophysiologic effect was 54.6 +/- 15.2 ng/ml. We conclude that at this dose, intravenous metoprolol significantly prolongs sinus cycle length and AV nodal conduction, may modestly increase atrial and ventricular refractoriness, and appears to have electrophysiologic potency similar to propranolol. It is well tolerated following intravenous administration and may be of particular value in the acute treatment of supraventricular tachycardia when beta-receptor selectivity is desired.     

Effects of digitalis on atrial vulnerability

The effects of digitalis on vulnerability to atrial fibrillation and flutter were assessed in man, using the model of repetitive atrial firing initiated by post-drive atrial extrastimulation. Nine patients without heart failure or significant mitral valve disease were tested before and 30 minutes after the administration of 0.01 mg/kg ouabain. When repetitive firing was manifested by flutter, neither the flutter cycle length nor the interval from the initiating beat to the first flutter beat was consistently altered by ouabain. Repetitive firing was found at the atrial site with the shortest functional refractory period. The vulnerable zone bordered this refractory period. The functional refractory period was lengthened after ouabain, from 231 +/- 13 to 246 +/- 15 msec (mean +/- standard error of the mean) (P less than 0.025). Partly because of prolonged refractoriness, the vulnerable zone was curtailed by ouabain, from 32.2 +/- 5.7 to 9.4 +/- 4.6 msec (P less than 0.001). This result suggests a protective effect of digitalis against atrial fibrillation and flutter independent of its hemodynamic actions.     

Beat-to-beat changes in atrioventricular nodal excitability and its modulation by concealed conduction during functional 2:1 block in man

An atrial pacing model of functional 2:1 block was used in 10 patients to investigate for the first time the electrophysiologic properties of the human atrioventricular node during intermittent conduction. By varying the terminal portion of the 2:1 atrial train and using the extrastimulus technique, we characterized atrioventricular nodal (AVN) conduction and refractoriness after five different methods of AVN activation: a conducted beat (method I), a conducted beat with omission of the prior blocked beat (method II), a blocked beat (method III), a blocked beat "converted" to one that conducts by omission of the prior conducted beat (method IV), and finally, 1:1 conduction at twice the cycle length of the 2:1 train (control method V). Observed AVN conduction times obeyed the following relationship: method I greater than method II greater than method V, indicating a cumulative effect of concealed penetration by the blocked beats. During 2:1 block, the AVN effective refractory period (ERP) alternated with a mean beat-to-beat difference of at least 100 msec, due mostly to marked ERP abbreviation during AVN activation by method III (vs both 2:1 train cycle length and activation by method V). Concealed penetration by the blocked beat prolonged AVN ERP for the propagated beat (vs that with methods II and V), but to a lesser extent than conduction time was increased. Moreover, the AVN recovery curve with method I was displaced upward and to the right compared with that with methods II to V.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effect of phenylephrine infusion on atrial electrophysiological properties.

OBJECTIVE: To determine the effect of changes in autonomic tone induced by phenylephrine infusion on atrial refractoriness and conduction. DESIGN: Left and right atrial electrophysiological properties were measured before and after a constant phenylephrine infusion designed to increase sinus cycle length by 25%. SUBJECTS: 20 patients, aged 53 (SD 6) years, undergoing electrophysiological study for investigation of idiopathic paroxysmal atrial fibrillation (seven patients) or for routine follow up after successful catheter ablation of supraventricular tachycardia (13 patients). MAIN OUTCOME MEASURES: Changes in left and right atrial effective refractory periods, atrial activation times, and frequency of induction of atrial fibrillation. RESULTS: Phenylephrine (mean dose 69 (SD 18) mg/min) increased mean blood pressure by 22 (12) mm Hg (range 7 to 44) and lengthened sinus cycle length by 223 (94) ms (20 to 430). Left atrial effective refractory period lengthened following phenylephrine infusion from 250 (25) to 264 (21) ms (P < 0.001) but there was no significant change in right atrial effective refractory period: 200 (20) v 206 (29), P = 0.11. There was a significant relation between the effect of phenylephrine on sinus cycle length and on right atrial refractoriness (r = 0.6, P = 0.005) with shortening of right atrial refractoriness in patients with the greatest prolongation in sinus cycle length. During phenylephrine infusion, the right atrial stimulus to left atrial activation time at the basic pacing cycle length of 600 ms was unchanged, at 130 (18) v 131 (17) ms, but activation delay with a premature extrastimulus increased: 212 (28) v 227 (38) ms, P = 0.002. Atrial fibrillation was induced by two of 58 refractory period measurements at baseline and by 12 of 61 measurements during phenylephrine infusion (P < 0.01). Phenylephrine increased the difference between left and right atrial refractory periods by 22.8 (19.4) ms in the five patients with induced atrial fibrillation after phenylephrine compared to 0.9 (16.2) ms in the 13 patients without induced atrial fibrillation after phenylephrine infusion (P = 0.02). CONCLUSIONS: Phenylephrine infusion increased left atrial refractoriness and intra-atrial conduction delay following a premature right atrial extrastimulus. Induction of atrial fibrillation during phenylephrine infusion was associated with non-uniform changes in atrial refractoriness. These data support the concept that changes in autonomic tone may precipitate atrial fibrillation in susceptible individuals.     

Effects of proximal intra-atrial Wenckebach on distal atrioventricular nodal, and His-Purkinje, block with special reference to the theory of alternating Wenckebach periods

Intra-atrial Wenckebach patterns of stimulus-to-response intervals coexisting with distal, A-V nodal, and His-Purkinje, blocks occurred in eight patients during high right atrial stimulation at rapid rates. In two patients with 2:1 St-H block and in two patients with 4:1 St-V block, an increase in the degree of block occurred when the proximal intra-atrial Wenckebach cycle was completed with the stimulus which otherwise would have been propagated to the distal levels. However, the degree of block did not increase when the intra-atrial Wenckebach terminated in distally blocked stimuli. In one patient progression of 4:1 into 5:1 St-V block was due to the association of intra-atrial Wenckebach with alternating 2:1 block at the A-V nodal, and His-Purkinje, levels. Contrasting with most reports dealing with the mechanisms of alternating Wenckebach in a single structure, this study permitted the determination of the boundaries between proximal and more distal levels. It also showed that alternating Wenckebach cycles (of St-H intervals) ending with two consecutively blocked stimuli could result from the association of proximal intra-atrial Wenckebach with distal, A-V nodal Wenckebach, or abortive AW, cycles. The electrophysiology of documented two, or three, level block in different structures has validated previously made assumptions regarding multilevel block in a single structure.     

Electrophysiologic effects of atropine on atrioventricular conduction studied by His bundle electrogram

The electrophysiologic effects of atropine were studied with His bundle recordings in 14 patients. Administration of atropine, 0.5 mg intravenously, produced a moderate degree of sinus acceleration in all patients (average increase 20 percent over control rate). Atrioventricular (A-V) nodal conduction was enhanced during both sinus rhythm and at various paced atrial rates after administration of atropine. The paced atrial rates at which the A-V nodal Wenckebach phenomenon occurred were significantly higher after administration of the drug than before. Similar effects on retrograde conduction were observed during ventricular pacing. Atropine shortened both the functional and effective refractory periods of the A-V node but appeared to have no direct effect on either His-Purkinje conduction time or refractoriness. However, aberrant ventricular conduction and block within the His-Purkinje system increased during premature atrial stimulation after atropine administration. This was the result of shortening of the functional refractory period of the A-V node by atropine, which produced significantly shorter H₁–H₂ intervals. The effect of atropine on the electrophysiologic properties of the A-V conducting system was important in interpreting the conversion of a type I gap in A-V conduction to a type II gap.     

Influence of pacemaker-induced tachycardia with A-V block on left ventricular blood velocity in man.

Phasic instantaneous left ventricular blood velocity was measured by radiotelemetry in 28 subjects with a Doppler ultrasonic flowmeter catheter during atrial pacing and induced A-V block Type I Wenckebach A-V block with conduction ratios of 9:8 or lower generally produced a stepwise reduction of peak left ventricular blood velocity in relation to shortened R-R intervals. Longer Wenckebach periods resulted in little or no blood velocity alteration during 1:1 A-V conduction. Those beats following a blocked atrial depolarization were associated with augmented blood velocities. In three subjects, bigeminal periods of 3:2 A-V block resulted in larger left ventricular blood velocities when compared with 2:1 A-V block, despite identical R-R intervals following the blocked P wave. This latter phenomenon was attributed to diastolic augmentation of left ventricular contraction following the second and hemodynamically ineffective beat during 3:2 A-V block. Three patients manifested true blood velocity alternation during second-degree A-V block and changing R-R intervals. The variations in peak left ventricular blood velocity observed during atrial pacing and A-V block are related to changing inotropic state and cycle length dependent alterations of left ventricular diastolic filling.     

A second zone of compensation during atrial premature stimulation: Evidence for decremental conduction in the sinoatrial junction

125 consecutive patients with premature atrial stimulation were studied. Three demonstrated sinus node return cycles that were fully compensatory following premature atrial stimuli delivered early in diastole. This second zone of compensation was unaccompanied by significant alterations in the post-return cycle lengths or in P-wave morphology of the return cycle. To account for the occurrence of a complete compensatory pause following very early premature atrial depolarizations, we consider the possibility that retrograde conduction of the early atrial premature depolarization (APD) in the sinoatrial junction was delayed for a sufficient length of time to allow the sinus node to depolarize spontaneously on schedule. Collision between the APD and sinus beat would then occur despite the marked prematurity of the APD. Thus, the early APD had encountered the relative refractory period of the sinoatrial junction, suggesting that decrementai conduction takes place within the sinoatrial region in man. These findings imply that there is the potential for reentry in the region of the human sinoatrial junction.     

Transesophageal versus intracardiac atrial stimulation in assessing anterograde conduction properties of the accessory pathway in Wolff-Parkinson-White syndrome

Electrophysiologic intracardiac and noninvasive transesophageal testing, used to evaluate parameters of anterograde conduction across the accessory pathway, the refractory period and shortest atrial cycle length with 1:1 conduction over the pathway, were compared to assess the reliability of the noninvasive technique in identifying patients with Wolff-Parkinson-White syndrome, at risk of rapid ventricular response during atrial fibrillation when this arrhythmia is not inducible. Sixteen patients with Wolff-Parkinson-White syndrome were submitted both to invasive and transesophageal atrial stimulation. We evaluated both the functional and effective refractory periods of the accessory pathway, using the same drive cycle length, and the shortest cycle length with 1:1 atrioventricular conduction over the accessory pathway. There were no differences between the parameters obtained by intracardiac atrial stimulation and by transesophageal atrial stimulation. The two approaches correlated well: mean functional refractory periods of the accessory pathway were 285 +/- 42 msec and 289 +/- 32 msec, respectively (NS, r = 0.88); mean effective refractory periods of the accessory pathway were 267 +/- 41 msec and 271 +/- 32 msec, respectively (NS, r = 0.89); mean shortest cycle lengths with 1:1 conduction over the accessory pathway were 255 +/- 48 msec and 255 +/- 44 msec, respectively (NS, r = 0.94). These data demonstrate the reliability of transesophageal atrial stimulation in estimating the parameters for anterograde conduction across an accessory pathway. These results, and the already documented ability of transesophageal atrial stimulation to induce atrial fibrillation, suggest this noninvasive technique should be taken as a first approach in screening patients with Wolff-Parkinson-White syndrome.(ABSTRACT TRUNCATED AT 250 WORDS)     

Spontaneous termination of reentry after one cycle or short nonsustained runs. Role of oscillations and excess dispersion of refractoriness

This study describes factors that contribute to spontaneous termination of reentry lasting one to 10 cycles after induction by a single premature stimulus. Reentry was studied in vitro in rings of canine atrial tissue from around the tricuspid valve orifice. Activation was recorded from a circular array of 10 extracellular bipolar electrodes equally spaced around the ring. In some experiments, transmembrane or monophasic action potential recordings were made near critical sites. Termination of reentry within one cycle after induction was recorded 110 times in 11 of 35 experiments. Important factors contributing to termination were 1) an obligatory reversal of the activation sequence that resulted in a long coupling interval in the critical region beyond the site of unidirectional block after the premature stimulus and 2) much longer refractory periods limited to this critical region, which facilitated unidirectional block but contributed to termination when this region was first activated with a short coupling interval at the end of the first reentrant cycle. Termination of nonsustained reentry lasting longer than one cycle resulted from oscillations of conduction and refractoriness initiated by the abrupt shortening of cycle length after initiation of reentry. Oscillations of conduction resulted from interval-dependent conduction of reentrant impulses that encountered partially refractory tissue. For reentry to become sustained, the oscillations after induction of reentry must dampen. Thus, damped cycle length oscillations after induction may identify clinical tachycardias caused by reentry with a partially excitable gap.