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.     

Characteristics, Circuit, Mechanism, and Ablation of Reentry in the Rabbit Atrioventricular Node

INTRODUCTION: The circuitry underlying AV nodal reentry remains debated. We developed a model of AV nodal reentry and assessed the role of nodal inputs, compact node, and its posterior nodal extension (PNE) in this phenomenon. METHODS AND RESULTS: A fine scanning of short coupling interval range with an atrial premature beat consistently initiated slow-fast AV nodal reentrant beats that occurred 37+/-31 msec (mean+/-SD) after His-bundle activation in 11 of 16 consecutive rabbit heart preparations. The repeated testing (>40 times) of a chosen coupling interval within reentry window (6+/-9 msec, n = 11) yielded reentrant intervals that varied by 2+/-1 msec (mean SD for 40 beats+/-SD, n = 11). The breakthrough point of reentrant activation, as assessed from four perinodal sites, varied in different preparations from diffuse (4) to anterior (1), medial (3), or posterior (3); mean reentrant interval did not differ between perinodal sites. Antegrade perinodal activation pattern did not differ at reentrant versus nonreentrant coupling intervals and thus was not a primary determinant of reentry. A PNE ablation (n = 4) interrupted the slow pathway conduction and prevented reentry without affecting antegrade perinodal activation or fast pathway conduction. CONCLUSION: A reproducible model of AV nodal reentrant beats was developed and used to study underlying circuitry. The AV nodal reentry involves unaltered antegrade perinodal activation, slow PNE conduction and retrograde broad invasion of perinodal tissues starting at a preparation-dependent breakthrough point. A PNE ablation abolishes the reentry.     

Persistence of Single Echo Beat Inducibility After Selective Ablation of the Slow Pathway in Patients with Atrioventricular Nodal Reentrant Tachycardia:

Residual Slow Pathway Conduction Effects on AVN Function. Introduction : Residual slow pathway conduction with or without reentrant echo beats has been reported in 25% to 30% of patients undergoing ablation for AV nodal reentrant tachycardia (AVNRT).
Methods and Results : Fifty-eight consecutive patients (aged 45 ± 12 years) with slow-fast AVNRT underwent radiofrequency catheter ablation of the slow AV nodal pathway (SP). Residual slow-fast echo beat was documented in 21 (36%) of 58 patients (group A). The pre-and postablation AH intervals triggering the echo beats were similar (346 ± 8 msec vs 352 ± 6 msec, P = NS), as were the pre-and postablation echo zones (55 ± 6 msec vs 52 ± 5 msec, P = NS) and functional refractory period of the SP. A consistent prolongation of the AV nodal effective refractory period (AVN-ERP; from 265 ± 28 msec to 340 ± 50 msec, P < 0.001) and the Wenckebach cycle length (WBCL; from 298 ± 41 msec to 438 ± 43 msec, P < 0.001) was observed in all patients with abolition of SP conduction (group B). In group A patients, the prolongation of WBCL was less (285 ± 33 msec preablation, and 334 ± 41 msec postablation, P < 0.001). Additional pulses abolished the residual echo in 16 of 21 patients, and further prolongation of the AVN-ERP and WBCL comparable to those found in patients without a residual echo beat was observed. During 19 ± 8 months follow-up, no patient had clinical recurrence of AVNRT.
Conclusion : Residual single echo beat after SP ablation for AVNRT reflects the persistence of some portion of the SP with unchanged functional conduction properties whose prognostic significance is uncertain. A consistent increase of WBCL can be a reliable marker of complete abolition of slow pathway conduction and termination of AVNRT.     

Evidence for Multiple Atrio-AV Nodal Inputs in the Normal Dog Heart

Multiple Atrio-AVN Inputs in Dog Heart. Introduction : Complete AV block after combined fast pathway (FP) and slow pathway (SP) ablation is uncommon. The purpose of this study was to interrupt activation of these and additional inputs by placing a radiofrequency lesion across the interatrial septum between the FP and SP ablation sites.
Methods and Results : In eight anesthetized open chest dogs, FP ablation induced significant A-H prolongation (δA-H: 51±14 msec; P < 0.001) and a shift of earliest retrograde atrial activation from the anterior septum to the region of the coronary sinus (CS) os. Subsequently, ablation of the interatrial septum across the fossa ovalis was successful in 5 of 8 dogs, changing the sequence of atrial activation (A) so that A at the His-bundle electrogram, which initially preceded A at the CS os (18 ± 4 msec vs 46 ± 7 msec, P < 0.01), now followed CS os A (81 ± 31 msec vs 59 ± 20 msec, P < 0.05). Additional ablation of the SP caused a type II Mobitz AV block or complete AV block in 5 of 8 dogs. The four dogs with complete AV block sbowed a stable, high junctional escape rhytbm at a rate of 64 ± 16 beats/min. Pacing between the ablation lesions and the AV node in one dog showed 1:1 AV conduction and Wenckebach-type AV block indicating preserved AV nodal function. Histology showed necrotic changes in the FP and SP transitional cell zones and in the atrial tissue of the interatrial septum. However, the compact AV node. His bundle, and adjacent atria and transitional cells were undamaged.
Conclusion : There are additional AV nodal inputs in the interatrial septum in addition to the anterior FP and posterior SP inputs. Ablation of all of these may be required, if the aim is production of complete AV block proximal to the AV node with a high Junctional escape rhythm.     

Facilitation of A-V nodal reciprocation by procainamide.

Procainamide is known to depress conduction through the A-V node, and this property may facilitate the development of ventricular reciprocal beats or echoes. The occurrence of ventricular reciprocal beats was studied in 20 open-chest dogs before and after the administration of procainamide. While the ventricle was paced by basic stimuli, early ventricular premature beats were introduced at various coupling intervals to induce ventricular echoes. When ventricular echoes could be induced in a given heart, there was a continuous range of coupling intervals (or echo zone) within which ventricular echoes occurred. In the control state, no echo occurred in eight dogs and the echoes developed in 12 dogs with the mean echo zone of 38.3 msec. The effect of procainamide was studied at its therapeutic blood levels about 25 minutes after an intravenous injection of the drug in a dose of 10 mg. per kilogram. Of the first group of eight dogs, in which no echo occurred in the control state, four dogs developed ventricular echoes after the administration of procainamide with the mean echo zone of 29.3 msec. for the group. Of the second group of 12 dogs, in which ventricular echoes were induced in the control state, the administration of procainamide increased the echo zone in 10 dogs with the mean echo zone of 67.8 msec. for the group. Ventricular reciprocal beats were often sustained to produce short runs of supraventricular tachycardia in five dogs after the administration of procainamide. The results demonstrated a potentially deleterious effect of procainamide in facilitating the inducation of A-V nodal reciprocation by closely coupled ventricular premature beats.     

Electrophysiology of the Atrio-AV Nodal Inputs and Exits in the Normal Dog Heart

Ablation of Atrionodal Connections. Introduction : We studied the effects of selective and combined ablation of the fast (FP) and slow pathway (SP) on AV and VA conduction in the normal dog heart using a novel epicardial ablation technique.
Methods and Results : For FP ablation, radiofrequency current (RFC) was applied to a catheter tip that was held epicardially against the base of the right atrial wall. SP ablation was performed epicardially at the crux of the heart. Twenty-three dogs were assigned to two ablation protocols: FP/SP ablation group (n = 17) and SP/FP ablation group (n = 6). In 12 of 17 dogs, FP ablation prolonged the PR interval (97 ± 10 to 149 ± 22 msec. P < 0.005) with no significant change in anterograde Wenckebach cycle length (WBCL), Subsequent SP ablation performed in 8 dogs further prolonged tbe PR interval and the anterograde WBCL (117 ± 22 to 193 ± 27, P < O.(M)5). Complete AV block was seen in I of 8 dogs, whereas complete or high-grade VA block was seen in 6 of 8 dogs. In the SP/FP ablation group, SP ablation significantly increased WBCL with no PR changes. Combined SP/FP ablation in A dogs prolonged the PR interval significantly, but no instance of complete AV block was seen. VA block was found in 50% of these cases. Histologic studies revealed that RFC ablation affected the anterior and posterior atrium adjacent to the undamaged AV node and His bundle.
Conclusion : Using an epicardial approach, combined ablation of tbe FP and SP AV nodal inputs can be achieved with an unexpectedly low incidence of complete A V block, although retrograde VA conduction was significantly compromised.     

Anterograde and retrograde bradycardiac block in the His-Purkinje system. Finding in a patient with acute myocardial infarction

A patient with an acute inferior myocardial infarction developed a complete atrioventricular block and intermitent periods of atrioventricular conduction with QRS complexes showing right bundle branch block associated with left anterior hemiblock. Recordings of the His bundle electrogram showed that the atrioventricular block was infrahisian and that in periods of resumed atrioventricular conduction, the His-ventricle (H-V) interval was long. Ventricular escape beats showed concealed conduction to the atrioventricular node. Anterograde atrioventricular conduction was always resumed through the left posterior division when the preceding division when the preceding intervals between ventricular escape beats and the atrium (V-A intervals) were shorter than 580 msec. The same phenomenon occurred with right ventricular pacing. A retrograde His potential could be observed. Retrograde conduction of ventricular escape beats and ventricular paced beats was blocked if the H-V interval and the interval between the His bundle and the ventricular paced beat (H-V interval) were long (more than 600 msec and 550 msec, respectively). The existence of an intermittent anterograde and retrograde bradycardiac infrahisian block was inferred from the previously mentioned data; a fixed retrograde atrial nodal block was also present.     

Electrophysiologic Characteristics and Radiofrequency Catheter Ablation in Atrioventricular Node Reentrant Tachycardia with Second-Degree Atrioventricular Block

Second-Degree AV Block During AVNRT. Introduction : Detailed electrophysiologic study of AV nodal reentrant tachycardia (AVNRT) with 2:1 AV block has been limited.
Methods and Results : Six hundred nine consecutive patients with AVNRT underwent electrophysiologic study and radiofrequency catheter ablation of the slow pathway. Twenty-six patients with 2:1 AV block during AVNRT were designated as group I, und those without this particular finding were designated as group II. The major findings of the present study were: (1) group I patients had better anterograde and retrograde AV nodal function, shorter tachycardia cycle length (during tachycardia with 1:1 conduction) (307 ± 30 vs 360 ± 58 msec, P < 0.001), and higher incidence of transient bundle branch block during tachycardia (18/26 vs 43/609, P < 0.001) than group II patients: (2) 21 (80.8%) group I patients had alternans of AA intervals during AVNRT with 2:1 AV block. Longer AH intervals (264 ± 26 vs 253 ± 27 msec, P = 0.031) were associated with the blocked beats. However, similar HA intervals (51 ± 12 vs 50 ± 12 msec, P = 0.363) and similar HV intervals (53 ± 11 vs 52 ± 12, P = 0.834) were found in the blocked and conducted beats; (3) ventricular extrastimulation before or during the His-bundle refractory period bundle could convert 2:1 AV block to 1:1 AV conduction.
Conclusions : Fast reentrant circuit, rather than underlying impaired conduction of the distal AV node or infranodal area, might account for second-degree AV block during AVNRT. Slow pathway ablation is safe and effective in patients who have AVNRT with 2:1 AV block.     

Clinical and Electrophysiologic Characteristics and Long-Term Efficacy of Slow-Pathway Catheter Ablation in Patients With Spontaneous Supraventricular Tachycardia and Dual Atrioventricular Node Pathways Without Inducible Tachycardia

Objectives. We sought to investigate the long-term efficacy of slow-pathway catheter ablation in patients with spontaneous, documented paroxysmal supraventricular tachycardia (PSVT) and dual atrioventricular (AV) node pathways but without inducible tachycardia.Background. The lack of reproduction of clinical PSVT by programmed electrical stimulation, which is not uncommon in AV node reentrant tachycardia (AVNRT), is a dilemma in making the decision of the therapeutic end point of radiofrequency catheter ablation.Methods. Twenty-seven patients (group A) with documented but noninducible PSVT and with dual AV node pathways were prospectively studied. Programmed electrical stimulation could induce a single AV node echo beat in 12 patients, double echo beats in 4 patients and none in 11 patients at baseline or during isoproterenol infusion. Of the patients in group A, 16 underwent slow-pathway catheter ablation and 11 did not. The clinical and electrophysiologic characteristics of the 27 patients were compared with those of patients with dual AV node pathways and inducible AVNRT (group B, n = 55) and patients with dual AV node pathways alone without clinical PSVT (group C, n = 47).Results. During 23 ± 13 months of follow-up, none of the 16 patients with slow-pathway catheter ablation had recurrence of PSVT. However, 7 of the 11 patients without ablation had PSVT recurrence at 13 ± 14 months of follow-up (p < 0.03 by Kaplan-Meier analysis). Compared with groups B and C, group A consisted predominantly of men who had better retrograde AV node conduction and a narrower zone for anterograde slow-pathway conduction.Conclusions. Slow-pathway catheter ablation is highly effective in eliminating spontaneous PSVT in which the tachycardia is not inducible despite the presence of dual AV node pathways.     

Initiation of atrioventricular nodal reentrant tachycardia in patients with discontinuous anterograde atrioventricular nodal conduction curves with and without documented supraventricular tachycardia: Observations on the role of a discontinuous retrograde conduction curve

To evaluate factors playing a role in initiation of atrioventricular (AV) nodal reentrant tachycardia utilizing anterogradely a slow and retrogradely a fast conducting AV nodal pathway, 38 patients having no accessory pathways and showing discontinuous anterograde AV nodal conduction curves during atrial stimulation were studied. Twenty-two patients (group A) underwent an electrophysiologic investigation because of recurrent paroxysmal supraventricular tachycardia (SVT) that had been electrocardiographically documented before the study. Sixteen patients (group B) underwent the study because of a history of palpitations (15 patients) or recurrent ventricular tachycardia (one patient); in none of them had SVT ever been electrocardiographically documented before the investigation. Twenty-one of the 22 patients of group A demonstrated continuous retrograde conduction curves during ventricular stimulation. In 20 tachycardia was initiated by either a single atrial premature beat (18 patients) or by two atrial premature beats. Fifteen of the 16 patients of group B had discontinuous retrograde conduction curves during ventricular stimulation, with a long refractory period of their retrograde fast pathway. Tachycardia was initiated by multiple atrial premature beats in one patient. Thirteen out of the remaining 15 patients received atropine. Thereafter tachycardia could be initiated in three patients by a single atrial premature beat, by two atrial premature beats in one patient, and by incremental atrial pacing in another patient. In the remaining eight patients tachycardia could not be initiated. Our observations indicate that the pattern of ventriculoatrial conduction found during ventricular stimulation is a marker for ease of initiation of AV nodal tachycardia in patients with discontinuous anterograde AV nodal conduction curves.     

Susceptibility to atrial fibrillation and ventricular tachyarrhythmia in the Wolff-Parkinson-White syndrome: role of the accessory pathway

Clinical and electrophysiologic characteristics associated with spontaneous and inducible atrial fibrillation and ventricular tachyarrhythmia were assessed in 20 consecutive patients with Wolff-Parkinson-White (WPW) syndrome undergoing surgical division (n = 12) or transcatheter electrical ablation (n = 8) of accessory pathways. Patients with spontaneous atrial fibrillation were characterized by the trend (not significant) of a shorter antegrade accessory pathway effective refractory period (256 +/- 26 vs 303 +/- 109 msec). However, patients with and without spontaneous atrial fibrillation did not differ with respect to prevalence of structural heart disease (3 of 11 vs 2 of 9), intra-atrial conduction time (34 +/- 10 vs 32 +/- 10 msec), or interatrial conduction time (86 +/- 21 vs 88 +/- 17 msec). Thus, atrial and accessory pathway electrophysiologic properties (per se) were not clear determinants of susceptibility to atrial fibrillation. Among the 20 patients, 10 to 35 beats of nonsustained ventricular tachycardia (seven patients) or ventricular fibrillation (three patients) were induced at electrophysiologic study with one to three programmed extrastimuli. Clinically, a ventricular arrhythmia (ventricular fibrillation during atrial fibrillation) had occurred in only one of these patients. The discordance of these observations was significant (p less than 0.01). Patients with and without inducible ventricular arrhythmias were not distinguished by clinical factors or by electrophysiologic properties of the accessory pathway or ventricles. Accessory pathway conduction was completely or partially eliminated by ablation procedures in 14 of 20 patients. During a mean follow-up of 27 months, atrial fibrillation recurred in two patients with failed ablation procedures and in one patient with left atrial enlargement (despite accessory pathway division) (p = 0.019 vs pre-ablation). Ventricular arrhythmias remained inducible in two patients in whom accessory pathway ablation failed (p = 0.01 vs initial study). However, spontaneous ventricular tachyarrhythmias did not occur during follow-up. We conclude that susceptibility to spontaneous or inducible atrial fibrillation and ventricular tachyarrhythmia in patients with WPW syndrome and no organic heart disease depends primarily on the existence of a functional accessory pathway. These susceptibilities are eliminated by interruption of accessory pathway conduction. Ventricular tachyarrhythmias remain infrequent spontaneous events in the WPW syndrome. Their more frequent induction at electrophysiologic study is not predictive of clinical occurrence.     

Conversion of typical to "atypical" atrioventricular nodal reentrant tachycardia after radiofrequency catheter modification of the atrioventricular junction.

Typical atrioventricular (AV) nodal reentry tachycardia (AVNRT) is characterized by anterograde activation over a slowly conducting pathway and by retrograde activation through a rapidly conducting pathway. Preliminary reports suggest that radiofrequency catheter modification can eliminate typical AVNRT while preserving anterograde conduction. Radiofrequency catheter modification was used to treat 88 patients with typical AVNRT. After baseline electrophysiologic evaluation, the ablation catheter was positioned proximal and superior to the site of maximal His deflection. Radiofrequency energy was applied until there was significant attenuation of retrograde conduction, and elimination of AVNRT inducibility. Eighty-one patients were successfully treated and form the basis of this report. A new paroxysmal supraventricular tachycardia with RP greater than PR interval was induced at electrophysiologic testing after successful ablation in 9 patients (11%). Mean atrial-His activation time was 140 +/- 31 ms, and the ventriculoatrial activation time was 170 +/- 46 ms. This arrhythmia was induced only with ventricular pacing during isoproterenol infusion and appeared to be mediated by AV nodal reentry. New retrograde dual AV nodal physiology after modification was more frequent in patients with atypical tachycardia than in those without (4 of 9 vs 2 of 72; p less than 0.0001). Although none of the patients were treated, only 1 of 9 had an episode of spontaneous atypical tachycardia during a mean follow-up of 12 months. Results of this study confirm that typical AVNRT can be rendered noninducible without the complete destruction of reentrant pathways. Because induction of "atypical" AVNRT was not predictive of spontaneous arrhythmia recurrence, it should not be an indication for additional ablation sessions or long-term drug therapy.     

Selective radiofrequency ablation of the slow pathway for the treatment of atrioventricular nodal reentrant tachycardia. Evidence for involvement of perinodal myocardium within the reentrant circuit.

BACKGROUND. The circuit of atrioventricular (AV) nodal reentrant tachycardia may include perinodal atrial myocardium. Furthermore, in patients with dual AV nodal pathways, the atrial insertion of the slow pathway is likely to be located near the ostium of the coronary sinus, caudal to the expected location of the AV node. The present study was designed to evaluate the safety and efficacy of selective catheter ablation of the slow pathway using radiofrequency energy applied along the tricuspid annulus near the coronary sinus ostium as definitive therapy for AV nodal reentrant tachycardia. METHODS AND RESULTS. Among 34 consecutive patients who were prospectively enrolled in the study, the slow pathway was selectively ablated in 30, and the fast pathway was ablated in four. Antegrade conduction over the fast pathway remained intact in all 30 patients after successful selective slow pathway ablation. There was no statistically significant change in the atrio-His interval (68.5 +/- 21.8 msec before and 69.6 +/- 23.9 msec after ablation) or AV Wenckebach rate (167 +/- 27 beats per minute before and 178 +/- 50 beats per minute after ablation) after selective ablation of the slow pathway. However, the antegrade effective refractory period of the fast pathway decreased from 348 +/- 94 msec before ablation to 309 +/- 79 msec after selective slow pathway ablation (p = 0.005). Retrograde conduction remained intact in 26 of 30 patients after selective ablation of the slow pathway. The retrograde refractory period of the ventriculo-atrial conduction system was 285 +/- 55 msec before and 280 +/- 52 msec after slow pathway ablation in patients with intact retrograde conduction (p = NS). There were three complications in two patients, including an episode of pulmonary edema and the development of spontaneous AV Wenckebach block during sleep in one patient after slow pathway ablation and the late development of complete AV block in another patient after fast pathway ablation. Over a mean follow-up period of 322 +/- 73 days, AV nodal reentrant tachycardia recurred in three patients, all of whom were successfully treated in a second ablation session. CONCLUSIONS. Radiofrequency ablation of the slow AV pathway is highly effective and is associated with a low rate of complications.     

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.     

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.     

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.     

Vagal modulation of the rate-dependent properties of the atrioventricular node

Vagal effects on atrioventricular (AV) nodal conduction are accentuated by increases in heart rate. To establish the mechanism of these rate-dependent negative dromotropic actions, we studied the properties governing AV nodal adaptation to changes in heart rate in chloralose-anesthetized dogs in the absence and presence of bilateral cervical vagal nerve stimulation (20 Hz, 0.2 msec). Stimulation protocols were applied to evaluate the contributions of changes in AV nodal recovery, facilitation, and fatigue independently of each other. Vagal stimulation slowed AV nodal recovery in a voltage-dependent way, increasing the time constant of recovery (tau r) from 80 +/- 7 to 194 +/- 16 msec (mean +/- SEM, p less than 0.01) at the highest voltage studied. The facilitating effect of a premature (A2) beat was manifested by a leftward shift of the recovery curve (A3H3 versus H2A3) of a subsequent A3 beat. The magnitude of shift depended on the A1A2 coupling interval and was reduced by vagal stimulation at all A1A2 intervals (maximum shift: control, 63 +/- 12 msec; vagus, 24 +/- 11 msec; p less than 0.01). When recovery and facilitation were kept constant, abrupt increases in AV nodal activation rate caused a slow (tau = 75 beats) increase in AH interval (fatigue). Vagal stimulation increased the magnitude of this process (maximum: control, 11 +/- 2 msec; vagus, 27 +/- 3 msec; p less than 0.001), without altering its time course. At activation rates comparable to sinus rhythm in humans, vagal stimulation at an intermediate voltage increased the AH interval by 25 msec. As heart rate increased, vagally induced changes in dynamic processes amplified AH prolongation up to fivefold at maximum rate. The role of vagal changes in individual functional properties depended on heart rate, but slowing of recovery was the single most important factor, constituting over 50% of overall vagal action at rapid rates. We conclude that vagal stimulation alters the ways in which the AV node responds to changes in activation rate and that at rapid rates most of the negative dromotropic action of the vagus is due to changes in the AV nodal response to tachycardia. Alterations in rate-dependent AV nodal properties are a novel and potentially important mechanism through which interventions may affect AV nodal conduction.     

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.     

Irregularity of the ventricular rhythm during atrial fibrillation: effect of slow atrioventricular nodal pathway ablation.

BACKGROUND: The contribution of dual atrioventricular (AV) nodal pathway physiology to the irregularity of the ventricular rhythm during atrial fibrillation has not been clarified. HYPOTHESIS: This study was performed to assess the effects of slow AV nodal pathway ablation on the irregularity of the ventricular rhythm during atrial fibrillation. METHODS: Irregularity of the ventricular rhythm was quantified using analysis of heart rate variability. In 20 patients with AV nodal reentrant tachycardia, absolute heart rate variability during atrial fibrillation was quantified before and after slow AV nodal pathway ablation by the standard deviation of all NN intervals (SDNN). Relative heart rate variability was determined by computing the coefficient of variation, SDNN normalized for the standard deviation of the mean ventricular cycle length (MVCL-AF). RESULTS: The slope of the regression between MVCL-AF and SDNN was significantly more gradual after slow pathway ablation (slope 0.39 vs. 0.23, p < 0.001). Coefficient of variation increased in 12 patients with heart rates > 120 beats/min at baseline (18.6 +/- 3.9 vs. 22.1 +/- 2.7% MVCL-AF, p < 0.05), but decreased in 8 patients with heart rates < 120 beats/min at baseline (25.6 +/- 3.1 vs. 22.2 +/- 2.2% MVCL-AF, p = 0.05). Furthermore, coefficient of variation correlated with MVCL-AF only at baseline (slope 0.034, r = 0.66), but no relation was found after slow pathway ablation (slope 0, r = 0). CONCLUSIONS: Slow AV nodal pathway ablation alters the relation between absolute heart rate variability and mean ventricular rate during atrial fibrillation and eliminates cycle length dependency of relative heart rate variability. These data indicate that dual AV nodal pathway physiology contributes to the irregularity of the ventricular rhythm during atrial fibrillation.     

Electrophysiology of the Right Anterior Approach to the Atrioventricular Node:

Electrophysiology of Anterior AVN Input. Introduction: Previous reports have described electrophysiologic properties and rate-dependent responses in the transitional cell zone of the posterior AV nodal input (slow pathway). The purpose of this study was to investigate the electrophysiology of the anterior transitional cell zone (fast pathway) in vivo and in a Langendorff preparation perfused with a nonblood solution containing butanedionemonoxime to inhibit contraction. Methods and Results: In five anesthetized dogs, the His-bundle electrogram recorded from the aortic root included atrial activity in close proximity to the anterior limbus of the fossa ovalis. During decremental atrial pacing, the atrial potential exhibited amplitude alternans at a pacing cycle length (CL) of 135 ± 14 msec. In ten isolated pertused canine hearts, a bipctlar electrode catheter was positioned with its tip against the right anterior interatrial septum just superior to the tendon of Todaro. The AV Wenckebach CL (WCL) averaged 262 ± 21 msec. During further decreases in pacing CL, the bipolar atrial potential developed a 2:1 amplitude alternans (9/10 dogs) at CL = 168 ± 15 msec and then split into two components with subsequent 2:1 block between these components (10/10 dogs) at CL = 152 ± 19 msec. Radiofrequency ablation at this site in six dogs prolonged the stimulus to HB interval from 113 ± 19 to 151 ± 30 msec (P < 0.01) without changing the WCL, consistent with ablation of the fast AV nodal pathway. In six other isolated perfused canine hearts, an octapolar catheter (2-mm spacing) was positioned along the anterior limbus of the fossa ovalLs with the tip electrode located over the anterior portion (apex) of the triangle of Koch. The aforementioned 2:1 amplitude alternans occurred at a longer CL in the distal electrodes located at the tendon of Todaro than in the proximal electrodes at farther distances from the tendon of Todaro (185 ± 25 vs 171 ± 20 msec, P < 0.05), as did the 2:1 block between the two components (161 ± 18 vs 150 ± 18 msec, P < 0.05). Microelectrode recordings obtained adjacent to the catheter demonstrated 2:1 alternans and block patterns in the action potentials of transitional cells but not in atrial cells, which exhibited 1:1 conduction at all CL. Conclusions: The transitional cell zone in the anterior interatrial septum exhibits a specific rate-dependent, spatial gradient of conduction block, which can be recorded in bipolar electro-grams as well as microelectrode recordings. Electrophysiologic changes induced by radiofrequency ablation of this anterior atrial/transitional cell zone (corroborated by histology) provide strong presumptive evidence that this area constitutes all or a major part of the fast AV nodal pathway.