AV nodal dual pathway electrophysiology and Wenckebach periodicity

Dual Pathways and Wenckebach Periodicity. Introduction: The precise mechanism(s) governing the phenomenon of AV nodal Wenckebach periodicity is not fully elucidated. Currently 2 hypotheses, the decremental conduction and the Rosenbluethian step‐delay, are most frequently used. We have provided new evidence that, in addition, dual pathway (DPW) electrophysiology is directly involved in the manifestation of AV nodal Wenckebach phenomenon. Methods and Results: AV nodal cellular action potentials (APs) were recorded from 6 rabbit AV node preparations during standard A1A2 and incremental pacing protocols. His electrogram alternans, a validated index of DPW electrophysiology, was used to monitor fast (FP) and slow (SP) pathway conduction. The data were collected in intact AV nodes, as well as after SP ablation. In all studied hearts the Wenckebach cycle started with FP propagation, followed by transition to SP until its ultimate block. During this process complex cellular APs were observed, with decremental foot formations reflecting the fading FP and second depolarizations produced by the SP. In addition, the AV node cells exhibited a progressive loss in maximal diastolic membrane potential (MDP) due to incomplete repolarization. The pause created with the blocked Wenckebach beat was associated with restoration of MDP and reinitiation of the conduction cycle via the FP wavefront. Conclusion: DPW electrophysiology is dynamically involved in the development of AV nodal Wenckebach periodicity. In the intact AV node, the cycle starts with FP that is progressively weakened and then replaced by SP propagation, until block occurs. AV nodal SP modification did not eliminate Wenckebach periodicity but strongly affected its paradigm. (J Cardiovasc Electrophysiol, Vol. pp.1‐7)     

Extra AV nodal Wenckebach periodicity

Extra AV nodal Wenckebach periodicity was diagnosed in seven patients. The most frequent form of this conduction abnormality was an exit block. The underlying block was localized in the sinoatrial junction and in the atria in two patients; the AV junction and the ventricle were the site of the Wenckebach periodicity in one case each. In extra AV nodal exit block, the actual conduction delay is not seen on the ECG and the diagnosis is based on the progressive shortening of the P-P or R-R intervals followed by a pause which is less than twice the shortest P-P (R-R) interval depending on the level of the block. A Wenckebach periodicity in the bundle branches or within the reentry pathway each occurred in one patient. In these forms of Wenckebach periodicity, the diagnosis is established more readily because the conduction delay can be demonstrated on the surface ECG. The clinical significance of extra AV nodal Wenckebach periodicity is discussed.     

Unique electrophysiologic characteristics of atrioventricular nodal reentrant tachycardia with different ventriculoatrial block patterns: Effects of slow pathway ablation and insights into the location of the reentrant circuit

BACKGROUND: The electrophysiologic mechanisms of different ventriculoatrial (VA) block patterns during atrioventricular nodal reentrant tachycardia (AVNRT) are poorly understood. OBJECTIVES: The purpose of this study was to characterize AVNRTs with different VA block patterns and to assess the effects of slow pathway ablation. METHODS: Electrophysiologic data from six AVNRT patients with different VA block patterns were reviewed. RESULTS: All AVNRTs were induced after a sudden AH "jump-up" with the earliest retrograde atrial activation at the right superoparaseptum. Different VA block patterns comprised Wenckebach His-atrial (HA) block (n = 4), 2:1 HA block (n = 1), and variable HA conduction times during fixed AVNRT cycle length (CL) (n = 1). Wenckebach HA block during AVNRT was preceded by gradual HA interval prolongation with fixed His-His (HH) interval and unchanged atrial activation sequence. AVNRT with 2:1 HA block was induced after slow pathway ablation for slow-slow AVNRT with 1:1 HA conduction, and earliest atrial activation shifted from right inferoparaseptum to superoparaseptum without change in AVNRT CL. The presence of a lower common pathway was suggested by a longer HA interval during ventricular pacing at AVNRT CL than during AVNRT (n = 5) or Wenckebach HA block during ventricular pacing at AVNRT CL (n = 1). In four patients, HA interval during ventricular pacing at AVNRT CL was unusually long (188 +/- 30 ms). Ablations at the right inferoparaseptum rendered AVNRT noninducible in 5 (83%) of 6 patients. CONCLUSION: Most AVNRTs with different VA block patterns were amenable to classic slow pathway ablation. The reentrant circuit could be contained within a functionally protected region around the AV node and posterior nodal extensions, and different VA block patterns resulted from variable conduction at tissues extrinsic to the reentrant circuit.     

Maturational atrioventricular nodal physiology in the mouse

INTRODUCTION: Dual AV nodal physiology is characterized by discontinuous conduction from the atrium to His bundle during programmed atrial extrastimulus testing (A2V2 conduction curves), AV nodal echo beats, and induction of AV nodal reentry tachycardia (AVNRT). The purpose of this study was to characterize in vivo murine maturational AV nodal conduction properties and determine the frequency of dual AV nodal physiology and inducible AVNRT. METHODS AND RESULTS: A complete transvenous in vivo electrophysiologic study was performed on 30 immature and 19 mature mice. Assessment of AV nodal conduction included (1) surface ECG and intracardiac atrial and ventricular electrograms; (2) decremental atrial pacing to the point of Wenckebach block and 2:1 conduction; and (3) programmed premature atrial extrastimuli to determine AV effective refractory periods (AVERP), construct A2V2 conduction curves, and attempt arrhythmia induction. The mean Wenckebach block interval was 73 +/- 12 msec, 2:1 block pacing cycle length was 61 +/- 11 msec, and mean AVERP100 was 54 +/- 11 msec. The frequency of dual AV nodal physiology increased with chronologic age, with discontinuous A2V2 conduction curves or AV nodal echo beats in 27% of young mice < 8 weeks and 58% in adult mice (P = 0.03). CONCLUSION: These data suggest that mice, similar to humans, have maturation of AV nodal physiology, but they do not have inducible AVNRT. Characterization of murine electrophysiology may be of value in studying genetically modified animals with AV conduction abnormalities. Furthermore, extrapolation to humans may help explain the relative rarity of AVNRT in the younger pediatric population.     

Atrial pacing-induced alternating Wenckebach periodicity and multilevel conduction block in children

Multilevel block within the atrioventricular (AV) node has not been previously described in children. Six children with atrial pacing-induced repetitive block are presented. The conduction patterns satisfy the requisites for alternating Wenckebach periodicity or multilevel AV block. In 2 patients the block is documented in the AV node and infra-His region. In 4 patients multilevel block within the AV node is postulated by deductive reasoning. In this study, 2 patterns of alternating Wenckebach periodicity are reported for the first time: sequences of 3:1 block with progressive prolongation of the conducted impulses terminating in 4:1 block; and sequences of 2:1 block with progressive prolongation of the conducted impulses terminating in 2 series of 3:1 block, in which the first conducted impulse following the first 2 blocked beats is not the shortest one, whereas that following the second 2 blocked beats is the shortest.     

The electrophysiologic characteristics of the transplanted human heart

The electrophysiologic characteristics of the denervated human heart were assessed in 14 cardiac transplant recipients. Conduction intervals and refractory periods were measured at pacing cycle lengths of 500 msec and 400 msec. The faster pacing rate caused lengthening of the AH interval (83 +/- 23 msec to 116 +/- 41 msec, p less than 0.01) and shortening of the QT (338 +/- 27 msec to 313 +/- 22 msec, p less than 0.001) and JT (249 +/- 21 msec to 229 +/- 19 msec, p less than 0.001) intervals. There was no change in the SA, HV, or QRS durations. Wenckebach periodicity occurred at a longer cycle length in the retrograde than in the anterograde direction (409 +/- 96 msec vs 318 +/- 46 msec, p less than 0.01) and anterograde conduction was better than retrograde conduction in 13 of the 14 patients (93%). Increasing pacing cycle length resulted in shortening of the atrial effective (203 +/- 28 msec to 190 +/- 25 msec, p less than 0.001), ventricular effective (224 +/- 18 msec to 211 +/- 17 msec, p less than 0.01), and AV nodal functional (367 +/- 38 msec to 357 +/- 36 msec, NS) refractory periods. The AV nodal effective refractory period lengthened (294 +/- 31 msec to 314 +/- 52 msec, p less than 0.05). There was a close correlation between AV Wenckebach cycle length and the functional refractory period of the AV node (r = 0.853, p less than 0.001). These results are qualitatively and quantitatively similar to those reported in the innervated heart. The autonomic nervous system appears to have little influence on the resting electrophysiologic characteristics of the atrioventricular conduction system in the innervated heart.     

Comparative effects of adenosine triphosphate on accessory pathway and atrioventricular nodal conduction

Adenosine triphosphate (ATP) has potent negative dromotropic effects on the atrioventricular (AV) node, but variable effects on accessory pathway conduction have been described. The effects of an intravenous bolus injection of 8 mg ATP on accessory pathway and AV nodal conduction were determined during electrophysiologic testing with controlled atrial and ventricular rates. AV conduction was monitored during atrial or ventricular pacing at a constant cycle length, 30 msec longer than the cycle length at which block occurred. During atrial pacing antegrade block after administration of ATP occurred in 1 of 30 (3.2%) patients with accessory pathway conduction and 12 of 13 (92%) patients with AV nodal conduction (p less than 0.001). During ventricular pacing only 5 of 26 (16%) patients had accessory pathways blocked, whereas 25 of 35 (71%) patients with AV nodal conduction had block (p less than 0.001). Thus, failure of ATP to produce ventriculoatrial block identified the presence of an accessory pathway with a sensitivity of 84%, specificity of 71%, and predictive value of 72%. There was no correlation between accessory pathway properties and the effects of ATP. The effects of ATP on the AV node were concordant with the effects of a combination of verapamil and propranolol in 21 of 23 patients, suggesting that this dose ATP is an equipotent AV nodal blocker with a short duration of action. Thus, although the effects of ATP on accessory pathways and the AV node differ, block in ventriculoatrial conduction after administration of ATP cannot be used as the sole criterion to distinguish the mechanism of conduction.     

Antiarrhythmic and proarrhythmic properties of diazepam demonstrated by electrophysiological study in humans

We evaluated the electrophysiological parameters before and after the intravenous infusion of diazepam (0.2 mg/kg) in 20 cardiac patients to investigate the drug's antiarrhythmic effect. Diazepam did not significantly change the arterial pressure. After the intravenous infusion of diazepam, the sinus cycle length significantly shortened from 847 +/- 132 to 747 +/- 155 ms (p less than 0.01). No significant change in the maximal sinus node recovery time was noted. The AH interval at the atrial pacing length of 600 ms shortened significantly from 140 +/- 40 to 127 +/- 39 ms (p less than 0.05). However, there was no significant change after the administration of diazepam in the longest atrial pacing rate associated with Wenckebach conduction in the atrioventricular (AV) node, effective and functional refractory periods of the AV node, HV interval, and QRS width during ventricular pacing at the cycle length of 600 ms. The atrial and ventricular effective refractory periods remained unchanged after the administration of diazepam. Six of the eight patients who showed dual AV nodal refractory period curves in the control study did not demonstrate them after diazepam administration by increasing the atrial or AV node effective refractory period. Thus, diazepam showed significant electrophysiological effects of the heart including shortening of the sinus cycle length, improvement in AV node conduction, and no significant effect on the His-Purkinje or intraventricular conduction and refractoriness of the atrium, AV node and ventricle. On the other hand, diazepam may influence the inducibility of supraventricular reentrant tachycardia incorporating the AV node.     

Effects of beta-adrenergic receptor stimulation and blockade on rate-dependent atrioventricular nodal properties.

Recent work has shown that alterations in the dynamic atrioventricular (AV) nodal response to changes in heart rate can significantly modify AV nodal function. The present study was designed to evaluate the nature and potential importance of sympathetic regulation of the rate-dependent properties of the AV node. Selective stimulation protocols and mathematical formulations were used to independently quantify AV nodal recovery, facilitation, and fatigue in 12 morphine-chloralose-anesthetized dogs. Vagal effects were prevented by bilateral vagal transection and intravenous atropine, and the sinus node was crushed to allow a broader range of pacing cycle lengths. In seven dogs with sympathetic nerves intact, beta-adrenergic receptor blockade increased the recovery time constant (tau rec) for the conduction of premature test beats from 47 +/- 2 (mean +/- SEM) msec (control) to 62 +/- 1 msec (p less than 0.001), whereas isoproterenol decreased tau rec to 38 +/- 1 msec (p less than 0.001). In addition, beta-blockade increased the maximum amount of rate-dependent AV nodal fatigue from 7 +/- 1 msec (at a cycle length of 198 +/- 9 msec [control]) to 17 +/- 2 msec (p less than 0.001). In five dogs with decentralized stellate ganglia, tau rec was decreased from 71 +/- 3 msec (control) to 57 +/- 4 msec and 48 +/- 2 msec (p less than 0.001 for each) by left stellate ganglion stimulation at 5 and 10 Hz, respectively. Maximum fatigue was similarly reduced from 16 +/- 1 msec (control) to 12 +/- 2 msec (p = NS) and 8 +/- 1 msec (p less than 0.01), respectively. Stellate ganglion stimulation, isoproterenol, and beta-blockade did not alter AV nodal facilitation. A mathematical model incorporating quantitative indexes of AV nodal function accurately accounted for tachycardia-dependent increases in the atrial-His activation interval, which were enhanced by beta-adrenergic receptor blockade and reduced by isoproterenol. Furthermore, this model showed that beta-adrenergic effects were increased by increasing heart rate, with the majority of the rate-dependent action being due to changes in the time course of AV nodal recovery. We conclude that beta-adrenergic receptor stimulation alters functional properties that govern the AV nodal response to changes in heart rate. These changes in functional properties alter the ability of the AV node to conduct impulses during tachycardia and, as such, could play a major role in the ability of sympathetic stimulation to promote and beta-adrenergic receptor blockade to prevent the occurrence of AV nodal reentrant arrhythmias.     

Electrophysiologic effects of bepridil in the anesthetized dog studied by endocardiac electrodes

The electrophysiologic effects of bepridil in the anesthetized closed-chest dog were studied with intracardiac electrodes using the extrastimulus technique to measure the refractory periods of atria, atrioventricular (AV) junction and ventricles. Intravenous administration of 5 mg/kg of bepridil caused a reduction in sinus node rate and prolonged the sinus node recovery time. Refractory periods in the atrium, especially the effective refractory period, increased. Anterograde AV nodal conduction was slowed and refractoriness increased, often resulting in AV nodal Wenckebach periods, during atrial pacing, and retrograde conduction was always completely abolished. Refractory periods of the AV junction were altered in a comparable fashion to conduction through the AV node. No significant actions on conduction or the refractory period were noticed in the His-Purkinje system or the ventricle. The mechanism of action of bepridil seems to be correlated to its membrane effects, namely, inhibition of pathways responsible for the slow inward current, which explains its selective action on myocardial sites where this current is particularly involved.     

Atrioventricular nodal accommodation in isolated guinea pig hearts: physiological significance and role of adenosine

The progressive prolongation of atrioventricular node (AVN) conduction time to a new steady-state value caused by sudden and maintained increases in atrial rate is the most common form of AV nodal accommodation. This study was undertaken to 1) characterize AV nodal accommodation in isolated perfused guinea pig hearts, 2) investigate the influence of potential modulators of this phenomenon such as acetylcholine and adenosine, and 3) determine the physiological significance of AV nodal accommodation on cardiac function. Beat-by-beat changes in AVN conduction time caused by single- or multiple-step increases in atrial pacing rate were measured during control conditions and in the presence of atropine (1 microM), propranolol (1 microM), and the adenosine antagonist BW-A1433 (1 microM). BW-A1433 was the only intervention that significantly reduced the cumulative and frequency-dependent prolongation of AVN conduction time but this was only observed at atrial cycle lengths less than or equal to 170 msec. In addition, BW-A1433 shortened the Wenckebach cycle length from 163 +/- 2 to 153 +/- 2 during normoxia and from 172 +/- 3 to 164 +/- 4 during mild hypoxia. In contrast, dipyridamole (1 microM), an adenosine uptake blocker, markedly accentuated the AVN conduction time prolongation, accentuated the AV block associated with fast atrial rates, and significantly increased the Wenckebach cycle length. These effects of dipyridamole were prevented and antagonized by BW-A1433 and adenosine deaminase. When O2 supply was limited and at the same time demand increased secondary to fast atrial pacing, the rate of adenosine release increased from a control of 125 +/- 27 to 580 +/- 54 pmol/min/g. This was accompanied by a significant prolongation in AVN conduction time that invariably progressed to AV block. Once AV block occurred, O2 consumption decreased, O2 supply-to-demand ratio improved and the rate of adenosine release dropped to 310 +/- 61 pmol/min/g. Reversal of the AV block with adenosine antagonists resulted in a decrease in O2 supply-to-demand ratio and a severalfold increase in the rate of adenosine release. In this feedback system, adenosine signals the imbalance between O2 supply and demand, causes AV block and, thus, reduces demand to compensate for the limited O2 supply. On the other hand, adenosine deaminase and antagonists act as "error signals" by attenuating the effect of adenosine, whereas dipyridamole enhances the "gain" of the system by potentiating the effects of adenosine.(ABSTRACT TRUNCATED AT 400 WORDS)     

Sick sinus syndrome: the role of hypervagotonia

A 58-year-old man with persistent symptomatic sinus bradycardia (52 beats/min) showed a markedly prolonged postpacing pause (3240 msec) after atrial pacing at a cycle of 840 msec. In addition, Wenckebach block occurred following atrial pacing at a cycle length of 700 msec. After atropine (2 mg) postpacing pauses returned to normal value and type 1 second-degree AV block completely reversed to 1:1 AV conduction until paced rates greater than 140/min. It may be that in some patients marked and persistent vagal overactivity may predispose to "intrinsic" sinus node dysfunction; in later stages, sinus node function may paradoxically result unaffected by changes in autonomic tone.     

Ventriculo-atrial conduction in patients with normal and impaired atrio-ventricular conduction

Ventriculo-atrial (VA) conduction was studied in 133 patients with various kinds of arrhythmias using intracardiac electrograms and programmed stimulation. One-to-one VA conduction was observed during RV pacing at the rate just above the sinus rate in 6 of 31 patients (19.4%) with advanced AV block, in 7 of 26 patients (26.9%) with impaired AV nodal conduction, in 25 of 71 patients (35.2%) with normal AV nodal conduction and 3 of 5 patients (60%) with enhanced AV nodal conduction. However, the differences between these groups were not significant. There was no significant difference in either the AH block rate during RA pacing or the antegrade functional refractory period (FRP) of the AV node in patients with or without VA conduction, and the VA block rate during RV pacing was not significantly correlated with the AH block rate or the FRP of the AV node. VA conduction time (S-HRA) also showed no significant differences between these groups. The mean VA conduction time during RV pacing at rates of 60 to 80 bpm was 208 +/- 87 msec, ranging from 100 to 395 msec. In conclusion, AV conduction disturbances may influence VA conduction, but VA conduction cannot be predicted from antegrade conductivity.     

Electrophysiologic effects of intravenous magnesium in patients with normal conduction systems and no clinical evidence of significant cardiac disease

Parenteral magnesium has been used for several decades in the empiric treatment of various arrhythmias, but the data on its electrophysiologic effects in man are limited. We evaluated the electrophysiologic effects of magnesium sulfate (MgSO4) administration in eight normomagnesemic patients with normal mononuclear cell magnesium content, who had no clinically significant heart disease and had normal baseline electrophysiologic properties. After administration of intravenous MgSO4, serum magnesium rose significantly from 1.9 +/- 0.1 to 4.4 +/- 1.7 mg/dl (p less than 0.02). During a maintenance magnesium infusion, we observed significant prolongation of the ECG PR interval (145 +/- 18 to 155 +/- 26 msec, p less than 0.05), AH interval (77 +/- 27 to 83 +/- 26 msec, p less than 0.002), antegrade atrioventricular (AV) nodal effective refractory period (278 +/- 67 to 293 +/- 67 msec, p less than 0.05), and sinoatrial conduction time (60 +/- 34 to 76 +/- 32 msec, p less than 0.02). No significant effect was observed on sinus cycle length, sinus node recovery time, intra-atrial or intraventricular conduction times, QRS duration (during both sinus rhythm and ventricular pacing), QT interval, HV interval, paced cycle length resulting in AV nodal Wenckebach block, AV nodal functional refractory period, retrograde ventriculoatrial (VA) effective refractory period, or atrial and ventricular refractory periods. These findings, in conjunction with the demonstrated ability of magnesium to block slow channels for sodium movement, may provide an explanation of the mechanism by which magnesium exerts its effect in the treatment of atrial and junctional arrhythmias.     

Dynamic Behavior of the Atrioventricular Node:

AV Nodal Memory. The wide variety of delays that the atrioventricular node can generate in response to an increased rate are explained by dynamic interactions between the three intrinsic properties of recovery, facilitation, and fatigue. The functional model presented suggests that any deviation of nodal conduction time from its minimum basal value represents, at any given time, the net sum of the effects produced by these properties. When a constant fast atrial rate is suddenly initiated, the node first "sees" a shortening in recovery time and responds by an increase in conduction time. This increase further shortens the recovery time of the ensuing beat, which is accordingly further delayed, and so on until a steady state is reached or a block occurs. However, these events do not occur alone. The second heat al the fast rate is conducted with a shorter conduction time than expected from the recovery time alone, and is therefore facilitated. These facilitatory effects develop within one short cycle and dissipate within one long cycle. They affect increasingly the conduction time of beats occurring with shorter cycle lengths. While steady-state effects of recovery and facilitation occur within seconds, nodal conduction time continues to increase slowly over several minutes when a rapid rate is maintained. This effect is attributed to fatigue, which develops and dissipates with a slow, symmetric time course. The dynamics of these properties can now be directly studied with selective stimulation protocols, and have many implications for the understanding of nodal behavior in the context of supraventricular tachyarrhythmias.     

Ventricular echo beats during ventricular pacing or junctional bradycardia: studies in the normal canine heart

In 15 adult dogs ventricular echoes were elicited during sinus rhythm by incremental ventricular pacing and during atrioventricular (AV) junctional rhythm by depressing simultaneously AV junctional automaticity and retrograde AV nodal conduction. Concomitant slowing of AV junctional automaticity and conduction was achieved by selective intranodal administration of verapamil. In three dogs incremental pacing from either ventricle failed to retrogradely activate the atria, and in each case the site of block was found to be in the AV node. In two dogs with retrograde atrial capture there was little or no rate-dependency of retrograde ventriculoatrial (VA) conduction. During incremental ventricular pacing a single ventricular echo beat was observed in 10 of the 12 dogs that had atrial capture, and the atrium appears to be an essential link in the production of each ventricular echo. Ventricular echo occurred when the time allotted for retrograde VA conduction amounted to 70 +/- 4% of the duration of the ventricular pacing cycle length. During AV junctional rhythm, a single ventricular echo was elicited in half of the dogs and in each of those cases intranodal verapamil produced a profound depression of retrograde VA conduction. These experiments suggest that retrograde AV nodal longitudinal dissociation occurs in the slow current-dependent cells of the AV node.     

Site of conduction delay and electrophysiologic significance of first-degree atrioventricular block in children with heart disease

Associated electrophysiologic abnormalities and site of delay were studied in 20 patients, aged 1.5 to 16.5 years, with congenital heart disease and first-degree atrioventricular (AV) block (PR interval above the 98th percentile for age and heart rate). Eight of the 20 patients with first-degree AV block were studied after 1 or more cardiovascular operations. Refractory periods of the atrium, AV node, His-Purkinje system and ventricle were determined. As a further test for AV nodal integrity, rapid atrial pacing was performed and the cycle at which Wenckebach periodicity occurred was noted. Four groups were identified. Group I included 4 patients (20%) with intraatrial conduction delay (long PA interval). Three patients had depressed sinus nodal function and 1 had depressed AV nodal function. Group II included 7 patients (35%) with AV nodal delay (long AH interval). One patient had sinus nodal depression and 2 had AV nodal depression (prolonged AV nodal refractory period or Wenckebach at a long paced cycle length). Group III included 3 patients (15%) with His-Purkinje delay (long HV interval). Measured functions were normal in all patients. Group IV included 6 patients (30%) with normal or high normal intracardiac intervals with long PR. One patient had sinus nodal dysfunction, 2 patients had long atrial refractory periods, 1 had AV nodal depression; 2 had long refractory period of the His-Purkinje system, and 1 had long ventricular refractory period. Atrial flutter was induced in 1 patient.(ABSTRACT TRUNCATED AT 250 WORDS)     

Modification of human atrioventricular nodal function by selective atrioventricular nodal artery catheterization

The hypothesis that human atrioventricular (AV) nodal function can be modulated selectively with a new technique of AV nodal artery catheterization was tested in eight subjects referred for diagnostic cardiac catheterization or electrophysiological studies. Three patients had no history of arrhythmias. Three patients had supraventricular tachycardia (SVT) due to reentry confined to the AV node (AVNRT). One patient had SVT due to reentry over a concealed AV bypass tract (AVRT-CBT), and one patient had nonsustained ventricular tachycardia. In each subject, sinus cycle length, AH interval, HV interval, AV nodal effective refractory period (AVN-ERP), and Wenckebach paced cycle length were measured in a control state. A flexible infusion catheter was then positioned selectively in the AV nodal artery of each subject. Through this catheter, a constant infusion of 0.1 mg/min procainamide at a flow rate of 0.125 ml/min (n = 1) or 50 micrograms/min acetylcholine at a flow rate of 0.25 ml/min (n = 4) was administered. Electrophysiological parameters were determined again during selective AV nodal artery drug infusion and during infusion of saline at identical rates. Two subjects developed transient AV nodal block during selective AV nodal catheterization alone and did not receive an infusion of drug or saline. A stable position of the AV nodal artery catheter could not be achieved in one other subject, who also received no drug or saline. In the other five subjects, drug infusion caused an increase in AVN-ERP from a control value of 312 +/- 52 msec to a value of 543 +/- 228 msec (p less than 0.05) and an increase in Wenckebach paced cycle length from a control value of 360 +/- 47 msec to a value of 572 +/- 217 msec (p less than 0.05). These parameters were unchanged from control during selective saline infusion. In two patients with AVNRT, drug infusion abolished SVT by causing complete blockade of ventriculoatrial conduction as well as lengthening of anterograde AVN-ERP. In the patient with AVRT-CBT, drug infusion abolished SVT by preventing repetitive anterograde AV conduction. Saline had no effect on SVT inducibility. Selective AV nodal artery catheterization enables AV nodal function to be modulated exclusively. Delivery of ablative agents to the AV node by this technique may be useful in patients with refractory SVT.     

Atypical Wenckebach periodicity simulating Mobitz II AV block.

Eleven patients were studied and a total of 144 Wenckebach cycles in the AV node and 118 Wenckebach cycles in the His-Purkinje system were analysed to determine the incidence of typical and atypical Wenckebach periodicity, with particular emphasis on one variant of atypical Wenckebach that may simulate a Mobitz type II block. This pseudo-Mobitz II pattern was defined as a long Wenckebach cycle in which, at least, the last three beats of the cycle show relatively constant PR intervals (variation of no more than 0.02 s in surface leads and no more than 10 ms in His bundle electrograms) and in which the PR interval immediately following the blocked beat is shorter than the PR interval before the block by 0.04 s or more. Atypical Wenckebach cycles were found to be more common than the typical variety at both the AV node (67%) and His-Purkinje system (69%). The pseudo-Mobitz II pattern was seen in 19 per cent of atypical AV nodal Wenckebach periods and in 17 per cent of atypical His-Purkinje system Wenckebach cycles. The need to discern a ''classical'' Mobitz II block from a pseudo-Mobitz II pattern, especially in the setting of an acute inferior myocardial infarction, is emphasised.     

Atrioventricular nodal tachycardia in the absence of retrograde conduction

A patient with atrioventricular (AV) nodal reentrant tachycardia assessed by electrocardiographic and electrophysiological criteria is described. During ventricular pacing, retrograde conduction was absent at the longest cycle length tested with the site of block determined to be the AV node by concealed conduction criteria. These findings localize the tachycardia circuit above the His bundle and exclude a His-atrial bypass tract as the retrograde limb of the tachycardia circuit in this patient.