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)     

An analysis of Wenckebach periodicity

His bundle electrograms of 40 patients developing Wenckebach block during atrial pacing and four with spontaneous Wenckebach block above the His were reviewed to determine the frequency of classical Wenckebach periodicity. Thirty patients had 143 Wenckebach cycles that were suitable for analysis. Cycles were evaluated for the following features: 1) the first A-H interval as the shortest, 2) the first R-R interval as the longest, 3) the last R-R interval as the shortest, 4) a progressive diminution of the increment of A-H interval prolongation, 5) a progressive diminution of the R-R interval and 6) the R-R interval containing the nonconducted A wave being equal to twice the A-A interval less the sum of the increments of A-H prolongation. Wenckebach cycles that occurred during atrial pacing were not significantly different from those that occurred spontaneously. Fifteen per cent of all cycles met all six criteria- 14% had five, 6% had four; 17% had three; 20% had two; 27% had one; and 1% had none. Short cycles were the most likely to show typical Wenckebach periodicity: 56% of the cycles with conduction ratios of 4:3, 28% with 5:4 and 4% with 6:5 met at least five criteria, whereas none of the 22 cycles having ratios 7:6 or greater had more than three features. The first A-H interval as the shortest was the most common feature occurring in 98% of cycles, whereas the features of a progressive diminution of the increments of the A-H interval prolongation or the progressive diminution of the R-R interval were the least common, occurring in 35% of cycles. These findings indicate, therefore, that classical Wenckebach periodicity is uncommon, especially when conduction ratios are 5:4 or greater. The implications of these observations and the suggested mechanisms are discussed and literature reviewed.     

Evaluation of five computer programs in the diagnosis of second-degree AV block.

Five electrocardiogram (ECG) analyzing systems were tested with a microcomputer-based ECG signal generator to assess the accuracy of the systems in interpreting Wenckebach periodicity. Although normal sinus rhythm with normal PR intervals and sinus rhythms with first-degree atrioventricular (AV) block were diagnosed by all five systems, second-degree AV block with classic Wenckebach periodicity was routinely misdiagnosed by four of the five systems. No system recognized the atypical Wenckebach periods in a total of 200 trials, misinterpreting the phenomenon as atrial fibrillation, supraventricular rhythm, sinoatrial block, and other rhythm disturbances. In advanced AV block and a variety of ventricular arrhythmias, none of the five systems diagnosed second-degree AV block with Wenckebach periods. Marked unsatisfactory performance with regard to the diagnosis of Wenckebach periodicity indicates the urgent need for accelerated and comprehensive testing of ECG diagnostic equipment. The present generating device was seen as an effective troubleshooter in optimizing the diagnostic competency of computerized ECG systems.     

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)     

Paradoxical Shortening of the Second PR Interval During 3:2 Atrioventricular Nodal Block

Paradoxical Shortening in Second-Degree AV Block. A patient with 3:2 second-degree AV block after acute inferior wall myocardial infarction showed consistent PR interval shortening on the second conducted beat in each periodicity. Intracardiac electrophysiologic evaluation revealed that the site of block was nodal. A typical Wenckebach pattern with prolongation of the AH interval was noted. The shorter PR resulted from a paradoxical shortening of the HV interval in the second beat, most likely due to supernormal conduction in the setting of concomitant trifascicular disease.     

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.     

Unusual Wenckebach phenomenon due to an atrial tachycardia arising from the apex of Koch’s triangle in the presence of dual AV nodal physiology

A case of a patient with narrow QRS tachycardia and without structural heart disease is presented. The electrophysiologic study revealed an atrial tachycardia in the presence of dual atrioventricular (AV) nodal physiology and AV block at suprahisian level, the latter two leading to an unusual Wenckebach periodicity. The entire septal area was mapped as was the coronary sinus (CS) os and the earliest atrial activation was found at the apex of Koch’s triangle in close vicinity to the His bundle (HB). Cryomapping at that point reproducibly terminated the tachycardia without impairing AV conduction. Cryoablation rendered the tachycardia non-inducible. Discontinuous AV conduction persisted but AV nodal reentrant tachycardia (AVNRT) was not inducible. Six months later the patient is arrhythmia-free.     

Reentrant and nonreentrant forms of atrio-ventricular nodal tachycardia mimicking atrial fibrillation

BACKGROUND: Atrial fibrillation (AF) manifests disorganized atrial activity and irregular R-R intervals on electrocardiogram (ECG). Variation in R-R intervals can also be seen with other supraventricular tachycardias that may mimic AF. OBJECTIVE: We report our observations on three patients who were referred to our center to undergo pulmonary vein (PV) isolation for erroneously diagnosed AF in the setting of dual atrio-ventricular (AV) nodal pathways manifesting as AV nodal reentrant tachycardia (AVNRT) and/or double response during sinus rhythm. METHODS AND RESULTS: These three subjects (two females) were derived from a group of 456 consecutive patients undergoing AF ablation at our center over a 3-year period. All three patients had been symptomatic for over 2 years, having failed two or more antiarrhythmic medications. In each case AF was initially diagnosed on ECG and/or recordings from ambulatory monitoring. However, in all three cases the correct diagnosis was established during the invasive electrophysiologic study. In one patient during the stimulation protocol, two narrow complex tachycardias were serially induced (cycle lengths: 305 and 360 msecs; VA time: 60 and 240 msecs). The latter was confirmed to be atypical AVNRT and during this tachycardia, block in upper pathway was observed. In the other two patients, sinus rhythm with repetitive runs of double response and isolated junctional beats were observed in the absence of retrograde conduction. Successful slow pathway modification was performed in each subject and all three patients have remained arrhythmia free over a mean follow-up of 31 +/- 16 months off antiarrhythmic medications. CONCLUSIONS: AF can be erroneously diagnosed in patients with dual AV nodal pathways manifesting double response and/or AVNRT. Incorporating a stimulation protocol as a part of the AF ablation procedure may help in diagnosing these rare clinical presentations that can be cured by slow pathway modification alone.     

房室结双径路传导所致特殊心电图改变

为了解房室结双径路传导所致的较为特殊心电图改变,对食管电生理检查中发现的双径路传导和房室结内折返性心动过速进行分析。发现:(1)双径路传导可以造成不同程度的假性房室传导阻滞,(2)双径路同步1:2房室传导可造成交接区和室性心律失常的假象,(3)在房室结内折返性心动过速发生上部和下部共同径路传导阻滞时又可使心电图表现复杂化。上述改变对进一步认识房室结双径路传导与心律失常的关系有重要意义,能显著提高对房室结双径路传导的正确诊断。     

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 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.     

Atrioventricular nodal reentrant tachycardia: studies on upper and lower 'common pathways'

Electrophysiologic studies were performed in 28 patients with documented atrioventricular (AV) nodal reentrant supraventricular tachycardia (SVT) to investigate the presence of AV nodal tissue situated between the tachycardia circuit and both the atrium (upper common pathway, UCP) and the His bundle (lower common pathway, LCP). All patients demonstrated a 1:1 AV relationship during SVT. The study protocol consisted of atrial then ventricular pacing at the SVT cycle length. UCPs were manifested in eight of 28 (29%) patients by either antegrade AV Wenckebach (six patients) or a paced atrium-His (AH) interval exceeding the AH in SVT (two patients, differences 5 and 9 msec). LCPs were manifested in 21 of 28 (75%) patients by either retrograde Wenckebach periodicity (two patients) or a paced HA interval exceeding the HA in SVT (19 patients, mean difference 25 +/- 20 msec). By these criteria, eight patients (29%) had evidence for both UCPs and LCPs. UCPs were more likely than LCPs to be manifested by Wenckebach criteria (p less than .05). Thus the AV nodal reentrant SVT circuit appears to be intranodal and is frequently surrounded by AV nodal tissue (UCP and LCP), antegrade and retrograde conduction properties of these common pathways are discordant in some cases, and conduction properties of UCP tissue differ from those of LCP tissue. These findings may have relevance in that the UCP or LCP may limit the ability of premature extrastimuli to penetrate the circuit to initiate or terminate AV nodal SVT.     

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.     

Rapid ventricular parasystole with possible multilevel exit block

A case of ventricular parasystole firing at the extremely rapid rate of 214 beats per minute in a 73 year old woman is described. Manifest cycle lengths of parasystolic complexes varied widely due to variable degrees of exit block, which could be best interpreted by the concept of multilevel block or alternating Wenckebach periodicity in the ventriculo-ectopic junction. Discontinuation of digoxin reduced the degree of exit block and unmasked parasystolic tachycardia.     

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.     

Stability of AV conduction in sick sinus node syndrome patients with implanted atrial pacemakers

Single-chamber atrial pacing is effective in the management of sinus node dysfunction, subject to the uncertainty of long-term atrioventricular conduction. Despite the accepted observation that many patients with sinus node dysfunction also have atrioventricular conduction disease, data do not exist on the development of atrioventricular block in those patients with permanent single-chamber atrial pacing. Of 70 patients who received single-chamber atrial pacing from 1967 to 1982 (mean duration of pacing was 33 months), only two patients of 58 (3.4%) of those with sinus node dysfunction developed atrioventricular (AV) block—after 14 months in one patient and after 23 months of successful atrial pacing in the other. None of the 12 patients paced for tachyarrhythmia management developed AV block. Of the 70 patients, 37 had assessment of AV conduction by incremental atrial pacing at the time of implant and 20 patients underwent atrial pacing on the basis of surface ECG and clinical judgment. Electrophysiologic studies were conducted only in those patients being paced for control of supraventricular arrhythmias. Only 5 of the 70 patients required conversion to ventricular pacing for technical difficulties; three of these conversions occurred in the early 1970's before the advent of atrial tined or J leads; one was for irreparable lead fracture and only one occurred in a patient with a newer design atrial lead. In conclusion, progression to AV block in patients with permanent atrial pacing is uncommon; formal electrophysiologic studies are necessary mainly in patients with supraventricular arrhythmias; and in the majority of patients, AV conduction can be assessed at the time of implant. Continued improvement in atrial leads should make atrial pacing even more successful.     

Asynchronous conduction in the human His bundle.

2 patients with symptoms of paroxysmal AV block showed widening, splitting, slurring and decreasing amplitude of the His potential. Concomitantly, this was followed by different patterns of bundle branch block. In one of the patients it was obvious that a left bundle branch block was related to a Wenckebach phenomenon in the His bundle, and in the other patient different bundle branch block patterns were related to the occurrence of the intra-His bundle conduction delay. It is suggested that the present electrophysiological findings reflect asynchronous conduction in the His bundle causing a critical conduction delay in parts of the bundle branches leading to bundle branch block.     

Significance of block distal to the His bundle induced by atrial pacing in patients with chronic bifascicular block.

Twenty-one of 496 (4%) patients with chronic bifascicular block, studied and followed prospectively, had block distal to the His bundle (BDH) induced by atrial pacing during initial electrophysiologic studies. In six, BDH was noted during pacing-induced atrioventricular (AV) nodal Wenckebach periods (at paced rates of 150--190 beats/min), with BDH in the short HH cycles after the AV nodal blocked P (lond cycle). The AH interval was normal in all six patients and HV was normal in four. None of the six patients has developed AV block during a mean follow-up of 5.33 +/- 0.48 years. In 15 patients, pacing-induced BDH was noted during intact AV nodal conduction (paced rate of 80--200 beats/min). The AH interval was prolonged in one, and HV was prolonged in 10 of the 15 patients. During a mean follow-up of 3.4 +/- 0.59 years, seven of these patients developed AV block, one had treadmill-provoked AV block, and two died suddenly (major morbid event in 10 of 15 patients). In conclusion, BDH induced by atrial pacing is an infrequent finding in patients with bifascicular block, and can be a functional as well as a pathologic response. The latter is associated with a high risk of major morbid events (AV block and sudden death).