Ventriculoatrial Block Research Articles

Differential Effects of Adenosine on Antegrade Fast Pathway, Antegrade Slow Pathway, and Retrograde Fast Pathway in Atrioventricular Nodal Reentry

Adenosine has a potent negative dromotropic effect. However, comparative effects of adenosine on the three pathways of atrioventricular (AV) nodal reentry remain unclear. In this study, we sought to determine the effects of adenosine on the antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AV nodal reentrant tachycardia (AVNRT). Twenty patients with common slow-fast AVNRT (mean cycle length 360 ± 49 ms) were studied. The effects of adenosine on the antegrade slow pathway and on the retrograde fast pathway conduction were determined during sustained AVNRT and constant right ventricular pacing at identical cycle lengths (mean 360 ± 49 ms), respectively. Incremental doses of adenosine were rapidly administered: initial dose of 0.5 mg, followed by stepwise increases of 0.5 or 1.0 mg given at 5-min intervals until termination of AVNRT or second-degree ventriculoatrial block occurred. After the antegrade slow pathway conduction was selectively and completely ablated by radiofrequency catheter ablation, the effect of adenosine on the antegrade fast pathway conduction was evaluated. The dose-response curve of adenosine and the dose of adenosine required to produce AV or ventriculoatrial block among the representative three conduction pathways were compared. The dose-response curve for the effect of adenosine on the antegrade fast pathway lies to the left and upward to that of the effect of adenosine on the antegrade slow pathway which in turn lies to the left and upward to that of the retrograde fast pathway. The mean dose of adenosine required to produce conduction block at antegrade fast, antegrade slow, and retrograde fast pathways were 1.4 ± 0.5, 4.2 ± 1.6, and 8.5 ± 2.6 mg, respectively (p < 0.01). Adenosine has a differential potency to depress antegrade fast, antegrade slow, and retrograde fast pathway conduction in patients with AVNRT. The depressant effect of adenosine on the antegrade fast pathway is more potent than that on the antegrade slow pathway which in turn is more potent than that on the retrograde fast pathway conduction.

Gender Differences in the Electrophysiological Characteristics of Atrioventricular Conduction System and their Clinical Implications

Objective - The underlying mechanisms of the differences in sex distribution of patients with atrioventricular (AV) nodal re-entrant tachycardia and Wolff-Parkinson-White syndrome are poorly understood. The objective of this study was to determine potential gender differences in the electrophysiological properties of the normal AV conduction system that may be attributable to differences in sex distribution. Design - The AV conduction properties were studied in 96 patients (52 men and 44 women) who underwent electrophysiological testing, 32 patients with atrial tachycardia, 39 with idiopathic ventricular tachycardia and 25 with unexplained palpitations or syncope. Results - The AH (83 - 15 ms) and His-ventricular intervals in men (42 - 6 ms) were significantly longer than in women (78 - 14, 38 - 6 ms, p < 0.05, respectively), as was the PR interval (160 - 17 vs 152 - 13 ms, p = 0.02). The effective refractory period of AV node in men (349 - 75 ms) was longer than in women (297 - 45 ms, p = 0.03). However, no significant difference was observed between men and women with respect to the incidence of AV nodal dual pathway and the maximum AH interval achieved during premature stimulation or incremental pacing. The AV block cycle length was significantly longer in men (371 - 76 ms) than in women (330 - 52 ms, p = 0.02). A longer ventriculoatrial block cycle length was also found in men than in women although not at a significant level (436 - 107 vs 384 - 90 ms, p = 0.08). In addition, men (23%) were twice as likely to have ventriculoatrial dissociation during ventricular pacing as women were (11%, p = 0.2). Conclusion - The data show that gender-related differences in AV conduction properties may be responsible for the differences in sex distribution observed in patients with AV nodal re-entrant tachycardia and those with ventricular pre-excitation.

High variability of retrograde fast pathway sensitivity to adenosine.

Adenosine is widely used as a tool to assess the effectiveness of radiofrequency ablation of concealed accessory pathways. The goal of this study was to determine the reliability of this test by studying the retrograde fast pathway sensibility in a large patient population with typical atrioventricular (AV) nodal reentry tachycardias. We sought also to determine whether AV nodal properties were predictive of a retrograde fast pathway sensitivity to adenosine. In all, 124 patients with inducible AV nodal reentrant tachycardia were included in this study. All patients received a clinically used standard dose of 12 mg adenosine during ventricular pacing, with 500 ms and a constant ventriculoatrial (VA) conduction via the fast pathway. Electrophysiologic parameters of the AV node were determined in all patients in order to correlate them with the adenosine sensitivity of the retrograde pathway. In 74 patients, the injection of 12 mg adenosine resulted in a transient VA block, whereas no VA block occurred in the remaining 50 patients. In two patients, concealed accessory pathways were unmasked after the injection of adenosine. The adenosine sensitivity of the retrograde fast pathway was associated with longer retrograde conduction times and cycle lengths during AV nodal reentrant tachycardias. This study shows a high variability of retrograde fast pathway sensitivity to adenosine. Thus, in 40% of patients the lack of VA block after adenosine injection is not specific for persistent accessory pathway function after radiofrequency ablation. Electrophysiologic properties of patients with AV nodal reentrant tachycardias were different in patients with and without adenosine-sensitive retrograde fast pathways, possibly indicating differential patterns of penetration of the retrograde fast pathway into the compact AV node.

Localization of the sites of conduction abnormalities in a mouse model of myotonic dystrophy.

A mouse strain lacking functional myotonic dystrophy protein kinase (DMPK) has recently been developed. DMPK-/- mice exhibit muscular and conduction abnormalities consistent with the disease; however, the site of abnormal cardiac conduction is unknown. Nine homozygous DMPK-/- mice and seven age matched wild-type (WT) controls underwent in vivo electrophysiologic studies using an endocardial 2-French catheter. Baseline intervals as well as Wenckebach and 2:1 cycle lengths were measured to assess AV and ventriculoatrial (VA) conduction. Effective refractory periods (ERP) and functional refractory periods were determined during atrial and ventricular premature stimulation. His-bundle recordings were obtained on all the studied animals (16/16). DMPK-/- mice had significantly prolonged PR (48.1 +/- 5.5 vs 40.9 +/- 3.9 msec, P = 0.010) and AH (36.7 +/- 4.0 vs 31.6 +/- 4.8 msec, P = 0.037) intervals compared to WT controls. HV intervals were very significantly prolonged as well (14.7 +/- 2.0 vs 10.3 +/- 0.8 msec; P < 0.0001). Three of 9 DMPK-/- and 1 of 7 WT mice exhibited VA block. Atrial ERP was reached before AV node ERP in 2 (22%) of 9 of the knockout mice and 5 (71%) of 7 of the controls (P = 0.06). Only one mouse (DMPK-/-) exhibited infra-Hisian block on premature atrial stimulation. In this mouse model of myotonic dystrophy, AV conduction abnormalities were localized to the supra-Hisian and infra-Hisian conduction tissues, with a higher predilection to the latter, a finding similar to the human form of the disease.

Cardiac electrophysiologic effects of norepinephrine in human beings

Background: The electrophysiologic effects of norepinephrine (NE) in human beings have not been previously described. Methods: The electrophysiologic effects of NE infused at a rate of 25 ng/kg/min were determined in 21 patients with a mean age of 41 ± 11 years and without structural heart disease who underwent an electrophysiology procedure. In a subgroup of 10 patients electrophysiologic parameters were measured at baseline, after the infusion of NE, and after administration of β-blockade while in continuous NE infusion. Results: The baseline NE plasma concentration of 298 ± 153 pg/ml increased to 708 ± 419 pg/ml after the infusion of NE. NE significantly increased the mean blood pressure, sinus cycle length, corrected sinus node recovery time, ventriculoatrial block cycle length, and the atrial and ventricular effective refractory periods. In a subset of 10 patients 0.2 mg/kg propranolol administered during continued infusion of NE resulted in a further increase in sinus cycle length, atrial-His interval, and ventricular refractoriness. Conclusion: A physiologic elevation in the plasma NE concentration results in a depression of sinus node function and atrioventricular conduction and in prolongation of atrial and ventricular refractoriness. Some of NE's effects are partially offset by β-adrenergic stimulation. (Am Heart J 1998;135:945-51.)

Narrow complex tachycardia with VA block: diagnostic and therapeutic implications.

To review our experience with cases of narrow complex tachycardia with VA block, highlighting the difficulties in the differential diagnosis, and the therapeutic implications. Prior reports of patients with narrow complex tachycardia with VA block consist of isolated case reports. The differential diagnosis of this disorder includes: automatic junctional tachycardia, AV nodal reentry with final upper common pathway block, concealed nodofascicular (ventricular) pathway, and intra-Hissian reentry. Between June 1994 and January 1996, six patients with narrow complex tachycardia with episodes of ventriculoatrial block were referred for evaluation. All six patients underwent attempted radiofrequency ablation of the putative arrhythmic site. Three of six patients had evidence suggestive of a nodofascicular tract. Intermittent antegrade conduction over a left-sided nodofascicular tract was present in two patients and the diagnosis of a concealed nodofascicular was made in the third patient after ruling out other tachycardia mechanisms. Two patients had automatic junctional tachycardia, and one patient had atrioventricular nodal reentry with proximal common pathway block. Attempted ablation in the posterior and mid-septum was unsuccessful in patients with nodofascicular tachycardia. In contrast, those with atrioventricular nodal reentry and automatic junctional tachycardia readily responded to ablation. The presence of a nodofascicular tachycardia should be suspected if: (1) intermittent antegrade preexcitation is recorded, (2) the tachycardia can be initiated with a single atrial premature producing two ventricular complexes, and (3) a single ventricular extrastimulus initiates SVT without a retrograde His deflection. The presence of a nodofascicular pathway is common in patients with narrow complex tachycardia and VA block. Unlike AV nodal reentry and automatic junctional tachycardia, the response to ablation is poor.

Variable effects of adenosine on retrograde conduction in patients with atrioventricular nodal reentry tachycardia.

Adenosine has been demonstrated to reliably produce transient block of atrioventricular nodal (AVN) conduction, and has been advocated as a method of differentiating retrograde conduction via the atrioventricular node from accessory pathway conduction. However, the response of retrograde AVN to adenosine in patients with typical atrioventricular nodal reentry tachycardia (AVNRT) remains unclear. We evaluated 13 patients (mean age 45 +/- 20 years) with typical AVNRT prior to AVN modification. During right ventricular pacing, a rapid bolus of adenosine (0.2 mg/kg; maximum 18 mg) was administered. Adenosine sensitivity, defined by transient ventriculoatrial block, was observed in six patients, while in seven patients ventriculoatrial conduction was unaffected. An adenosine bolus administered during sinus rhythm or atrial pacing resulted in antegrade atrioventricular block in all the adenosine resistant patients in whom this was performed (n = 6). Comparisons of AVN electrophysiological characteristics between the adenosine sensitive and adenosine resistant patients were performed. There was no difference with respect to ventriculoatrial effective refractory period, ventriculoatrial Wenckebach, AVNRT cycle length, and His to atrial echo interval in AVNRT. However, there was a trend toward a longer antegrade fast pathway ERP in the adenosine sensitive group (P = 0.07). Electrophysiological properties do not predict retrograde AVN adenosine sensitivity. Adenosine does not cause retrograde AVN block in all patients with AVNRT, and therefore cannot reliably distinguish between retrograde conduction via the AVN or an accessory pathway.

Fast pathway ablation in patients with common atrioventricular nodal reentrant tachycardia and prolonged PR interval during sinus rhythm.

This study aimed to clarify the safety and efficacy of selective fast pathway ablation in patients with atrioventricular nodal reentrant tachycardia and a prolonged PR interval during sinus rhythm. Such patients have been reported to have an increased incidence of complete atrioventricular block. In this study, the earliest retrograde atrial activation during atrioventricular nodal reentrant tachycardia and right ventricular stimulation was localized. Fast pathway ablation was then performed in five patients with the common form of atrioventricular nodal reentrant tachycardia and a prolonged PR interval. Three of the five patients had almost incessant atrioventricular nodal reentrant tachycardia. Radiofrequency catheter ablation induced a complete ventriculo-atrial block during right ventricular stimulation in four patients and a marked prolongation of ventriculo-atrial conduction during right ventricular stimulation in one. Non-inducibility of common atrioventricular nodal reentrant tachycardia with and without isoproterenol was achieved in all five patients. The PR interval increased from 254 +/- 53 ms to 276 +/- 48 ms and the atrio-His interval from 172 +/- 46 ms to 192 +/- 45 ms. Second- or third-degree atrioventricular block did not occur during the ablation procedure. During the followup of 19 +/- 20 months none of the patients developed symptoms suggestive of atrioventricular nodal reentrant tachycardia or evidence of second- or third-degree atrioventricular block. These data suggest that atrioventricular node (retrograde) fast pathway ablation can apparently be safely performed in patients with common atrioventricular nodal reentrant tachycardia and a prolonged PR interval during sinus rhythm.

Differential effects of adenosine on antegrade and retrograde fast pathway conduction in atrioventricular nodal reentry

Although adenosine depresses antegrade atrioventricular (AV) nodal conduction, the effects of adenosine on antegrade and retrograde fast pathway conduction in AV nodal reentry have not been determined. In 17 patients (five men, 12 women, mean age 49 +/- 12 years) with common slow-fast AV nodal reentrant tachycardia, the antegrade slow pathway conduction was selectively and completely ablated by radiofrequency catheter ablation while the antegrade and retrograde fast pathway conduction remained intact. During high right atrial pacing at a mean pacing cycle length of 474 +/- 36 msec, adenosine was rapidly injected intravenously at an initial dose of 0.5 mg followed by stepwise increases of 0.5 mg or 1.0 mg given at 5-minute intervals until second-degree AV block developed. During right ventricular apical pacing at the same pacing cycle lengths (mean 474 +/- 36 msec) as those in the study of antegrade conduction, intravenous injection of incremental doses of adenosine was repeated until ventriculoatrial (VA) block occurred. The adenosine-induced prolongation of VA conduction was also determined in the presence of verapamil (loading dose 0.15 mg/kg, maintenance dose 0.005 mg/kg/min) in seven of 17 patients. The dose of adenosine required to produce AV block, the increase in the atrio-His interval by 50% and the maximal response were 3.4 +/- 1.4 mg, 1.8 +/- 0.6 mg, and 58% +/- 5%, respectively. On the other hand, the dose of adenosine required to produce VA block, the increase in the VA interval by 50%, and the maximal response were 8.2 +/- 2.9 mg, 3.4 +/- 0.6 mg, and 20% +/- 5%, respectively, in the control and 3.7 +/- 0.5 mg, 3.5 +/- 0.7 mg, and 23% +/- 5%, respectively, in the presence of verapamil. In conclusion, adenosine has a differential potency to depress AV and VA conduction in patients with AV nodal reentry, with greater potency for slowing antegrade fast than retrograde fast pathway conduction. Verapamil had an additive effect to adenosine on slowing retrograde VA conduction, which further supports the evidence that the retrograde fast pathway in part involves an AV nodal-like structure.

Mechanism of QRS electrical alternans.

In patients with latent dual atrioventricular nodal pathways a 2:1 ventriculoatrial block often occurs during ventricular pacing and is generally associated with the concomitant appearance of QRS alternans. This type...

Electrophysiologic Properties of the Atrioventricular Node in Pediatric Patients

Objectives. The purpose of this study was to characterize anterograde and retrograde properties of the atrioventricular (AV) node in children and to determine the presence of ventriculoatrial (VA) conduction and dual AV node pathways.Background. Although AV node reentry is common in adults, it accounts for 13% of pediatric supraventricular tachycardia (SVT). The age-related changes in the AV node with development are poorly understood. The incidence of dual AV node pathways and VA conduction in the pediatric population is unknown.Methods. Electrophysiologic studies were performed in 79 patients with normal hearts and no evidence of AV node arrhythmias. Patients were classified into two groups by age: group I = 49 patients (0.39 to 12.8 years old, mean [±SD] age 8.5 ± 3.6); group II = 30 patients (13.4 to 20.0 years old, mean age 15.6 ± 1.8).Results. There was a significant difference (p < 0.05) in the cycle length (CL) at which anterograde AV block occurred between group I (305 ± 63 ms) and group II (350 ± 91 ms). Sixty-one percent of children had VA conduction with no age-related differences. There was no significant difference in the mean CL of retrograde VA block (360 ms). The incidence of dual AV node pathways in group I was 15% and 44% in group II (p < 0.05).Conclusions. These findings suggest that AV node electrophysiology undergoes maturational changes. The increase in AV node reentrant tachycardia in adults may relate to changes in the relative refractoriness and conduction of the AV node or to differences in autonomic input into the AV node that allow dual pathway physiology to progress to SVT.(J Am Coll Cardiol 1997;29:403–7)

Effects of adenosine triphosphate on ventriculoatrial conduction--usefulness and problems in assessment of catheter ablation of accessory pathways.

The effects of adenosine triphosphate (ATP) on ventriculoatrial (VA) conduction were examined before and after accessory pathway (AP) ablation, with emphasis on assessment of the complication of dual atrioventricular (AV) node pathway. By evaluating the differences in the response to ATP of APs and other pathways, we assessed the usefulness and problems of this method. Of 59 patients who underwent AP ablation, 31 showed pre-excitation and 28 had concealed APs. A dual AV node pathway was found in 9 patients (15.3%) before ablation. After ablation, a dual AV node pathway was newly found in 9 patients. Thus, the total number of patients with a dual AV node pathway was 18 (30.5%). VA conduction over APs was not blocked in 26 of 29 patients, but the remaining 3 APs were blocked transiently by ATP. ATP caused VA block over the AV node in 15 of 16 patients and a dual AV node pathway in all 11 patients. In contrast, VA conduction over the retrograde fast pathway was blocked in 9 of 14 patients with AV node re-entrant tachycardia. ATP has little effect on APs, so observation of the response to ATP provides a more reliable and useful means of evaluating successful ablation. With this method, however, it is important to consider the possibility of the presence of ATP-sensitive APs and ATP-resistant retrograde fast pathways. The influence of ablation-induced injury has not been fully clarified. It is therefore essential to take into account various data, including the comparison between data obtained before and after ablation.

Atrioventricular node properties in patients with accessory pathways

A study during the era of surgical ablation suggested that atrioventricular (AV) nodal conduction is faster in patients with accessory pathways than in controls. In the present study, AV nodal characteristics were studied in 30 patients who underwent radiofrequency ablationof an accessory pathway and compared to 23 control patients. Sinus cycle length, AH and HV intervals, AV block cycle length, ventriculoatrial (VA) block cycle length, AV nodal effective refractory period, and VA effective refractory periods were measured in control and postablation accessory pathway patients before and after autonomic blockade with 0.04 mg/kg of atropine and 0.2 mg/kg of propranolol. The mean sinus cycle length in the control and accessory pathway groups did not differ significantly at baseline (798 ± 211 and 766 ± 156 msec, respectively) or after autonomic blockade (654 ± 98 and 649 ± 108 msec, respectively). The mean AH interval in the accessory pathway group (77 ± 15 msec) was significantly shorter than in the control group (91 ± 22 msec; p < 0.05) at baseline; however, there was no difference after autonomic blockade. No other significant differences were observed between the accessory pathway and control groups. These results demonstrate that AV nodal properties of patients with accessory pathways are not significantly different from controls and suggest that previously reported differences may have been due to selection bias.

Prediction of Atrioventricular Block During Radiofrequency Ablation of the Slow Pathway of the Atrioventricular Node

Selective radiofrequency (RF) ablation of the slow pathway is an effective treatment for atrioventricular (AV) nodal reentry tachycardia. A previous report showed that rapid junctional tachycardia (JT) caused by RF associated with loss of ventriculoatrial (VA) conduction is related to increased risk for AV block. However, this can be difficult to detect during energy delivery, and more importantly, it cannot be measured before the onset of RF energy delivery. The aim of our study was to determine whether measurements made from electrograms could be used to predict the risk of AV block before RF energy is delivered. Fifty-eight patients underwent 63 selective slow pathway RF ablation procedures. In 46 (26.9%) of 172 JTs caused by RF, VA block was observed, and in 11 this was followed by AV block of various degrees. Electrograms before each application of RF were analyzed for the interval between the atrial signals in the His bundle catheter and in the distal mapping catheter [A(H)-A(Md)], the interval between the atrial signals in the His bundle catheter and in the proximal coronary sinus catheter [A(H)-A(CS)], the AV ratio, and the presence of a slow pathway potential or a fractionated atrial signal in the distal mapping catheter. Mean cycle length (CL) of JT was calculated if it consisted of at least 10 beats. These parameters were compared between patients with JT who developed VA block and subsequent AV block (group 1), patients with JT and VA block but without subsequent AV block (group 2), and patients with JT without VA block (group 3). The A(H)-A(Md) interval was significantly shorter in group 1 (17 +/- 8 ms) than in groups 2 (33 +/- 8 ms, P < .001) and 3 (32 +/- 10 ms, P < .001), whereas the A(H)-A(Md) intervals of groups 2 and 3 did not differ from each other. CL of JT, A(H)-A(CS) interval, AV ratio, presence of a slow pathway potential, or a fractionated atrial electrogram were not related to the occurrence of AV block. The A(H)-A(Md) interval provides an electrophysiological marker that can be used in addition to the radiological catheter position to assess the risk for AV block before onset of RF delivery. CL of JT and occurrence of VA block are not related to the risk of AV block.

Long term results of fast pathway ablation in atrioventricular nodal reentry tachycardia using a modified technique.

To assess immediate and long term success of "fast" pathway catheter ablation with graded use of radiofrequency energy in patients with classic atrioventricular nodal reentrant tachycardia (AVNRT) and evaluate clinical, procedure related, and electrophysiological features affecting long term results. 31 consecutive patients with classic AVNRT at electrophysiological study, who were candidates for radiofrequency ablation. Patients were followed for an average of 24 months after ablation. All studies and ablations were performed in an electrophysiological laboratory under fluoroscopic guidance using standard electrophysiological techniques. Radiofrequency application was performed at the site of proximal His bundle electrogram with A:V ratio of > 1. It was started at 10 W with increment of 5 W to a maximum of 25 W at 60 s. With the onset of junctional rhythm, atrial pacing was begun in order to monitor the PR interval. Application was terminated prematurely with a non-conducted P wave, continued prolongation of the PR interval beyond 50% of the baseline, or a threefold rise in impedance. Successful ablation was possible in 30/31 patients (97%) with an average of seven applications (range 1-10). It was associated with significant prolongation of PR interval (P < 0.001) and AV Wenckebach cycle length (P = 0.01). Ventriculo-atrial conduction was abolished in 24/30 patients (82%) with successful ablation. Two patients developed transient complete heart block (3 and 12 min) and one persistent right branch block. Four patients had late recurrence. Presence of ventriculo-atrial block was the only electrophysiological index predictive of long term success (P = 0.01). Graded use of radiofrequency energy and atrial pacing to monitor PR interval decreases the risk of atrioventricular block in patients undergoing fast pathway ablation for AVNRT. Ventriculo-atrial block is predictive of long term success and should be a preferred end point for fast pathway ablation.

An anatomically and electrogram-guided stepwise approach for effective and safe catheter ablation of the fast pathway for elimination of atrioventricular node reentrant tachycardia

We describe a new stepwise anatomically and electrogram-guided strategy for radiofrequency catheter ablation of the fast pathway. Anatomically and electrogram-guided approaches have been developed for slow pathway ablation in patients with atrioventricular (AV) node reentrant tachycardia; however, no stepwise systematic approaches exist for fast pathway ablation. Fifty-three patients (mean [+/- SD] age 43 +/- 11 years) with AV node reentrant tachycardia underwent attempted ablation of the fast pathway. The ablation catheter was initially positioned posterior and slightly superior to the site of the maximal His bundle recording region. At these sites, the amplitude of the local atrial potential was usually at least twice as high as the local ventricular potential, and a small proximal His bundle potential was recorded. When the first pulse was ineffective, the ablation catheter was repositioned stepwise slightly inferior to more midseptal sites. After a mean of 3.4 +/- 3.1 radiofrequency pulses (median 2, range 1 to 12), AV node reentrant tachycardia was noninducible in 51 patients (96%). No inadvertent complete AV block occurred. The AH interval was prolonged from 79 +/- 19 to 145 +/- 37 ms (p < 0.001). Thirty-eight patients (72%) developed complete ventriculoatrial block. Recording of a His bundle potential at the target site, stability of the local electrograms and occurrence of fast junctional rhythms during energy applications were more often observed at successful sites than transiently effective or noneffective sites. During a follow-up period of 12 +/- 7 months, 3 (6%) of 51 patients had a clinical recurrence of AV node reentrant tachycardia. Radiofrequency catheter ablation of the fast pathway using a combined anatomically and electrogram-guided stepwise approach is highly effective and safe. The safety of this approach seems to be due to the stable position of the ablation catheter at the interatrial septum, rather than across the tricuspid annulus, and the larger distance to the central body of the AV node and bundle of His.

Use of adenosine to identify patients at risk for recurrence of accessory pathway conduction after initially successful radiofrequency catheter ablation.

The use of adenosine after radiofrequency catheter ablation of accessory pathways was prospectively studied to determine its utility for identifying patients at risk for recurrence of accessory pathway conduction and to guide therapy that might reduce late recurrence in this group. Accessory pathway conduction recurs in 5%-12% of patients following initially "successful" radiofrequency catheter ablation. Adenosine may facilitate conduction over accessory pathways that have been modified by radiofrequency delivery, thus identifying patients at risk for recurrence. Radiofrequency catheter ablation was performed in 109 patients. Prior to ablation, 12-18 mg of adenosine was administered. After ablation, when all evidence of accessory pathway conduction remained absent for at least 30 minutes, adenosine 12-18 mg was again administered. Adenosine given prior to radiofrequency catheter ablation did not block accessory pathway conduction in any patient. Adenosine given after elimination of accessory pathway conduction induced complete atrioventricular and ventriculoatrial block in 95 patients; 11 (11.6%) subsequently had recurrence of accessory pathway function. Accessory pathway conduction was unmasked by adenosine in 12 patients (11.2%). After further deliveries of radiofrequency energy, 7 of these 12 patients subsequently demonstrated adenosine induced atrioventricular and ventriculoatrial block; 1 of these 7 patients experienced recurrence of accessory pathway conduction. The remaining 5 patients demonstrated persistent accessory pathway conduction only with adenosine; all experienced clinical recurrence of accessory pathway function. The use of adenosine after presumed successful radiofrequency catheter ablation may reveal persistent accessory pathway conduction. Elimination of this latent accessory pathway conduction reduces the risk for recurrence.

798-2 Differential Sensitivity of AV and VA Conduction to Adenosine in Humans

Studies in rat isolated hearts suggest that adenosine is more potent for slowing antegrade atrioventricular (AV) than retrograde ventriculo-atrial (VA) conduction. The potency (EC 50 ) and maximal effect (E max ) of adenosine to slow AV and VA conductions were determined in 16 patients (mean age 48 years). These patients were selected from a group that had a common form of AV nodal reentrant tachycardia who had prior to the study been subjected to selective radiofrequency ablation of the slow pathway conduction, but with intact antegrade and retrograde fast pathway conduction. During high right atrial and ventricular pacing at comparable cycle lengths (400–500 msec). adenosine was injected as an intravenous bolus at an initial dose of 0.5 mg followed by stepwise increase of 1 mg given every 5 minutes until AV or VA block occurred. The dose-response curves for adenosine-induced prolongation of AV and VA conduction time were determined. The 1:1 AV and VA conduction cycle lengths before injection of adenosine were 340 ± 50 and 326 ± 75 msec, respectively. Adenosine induced dose-dependent prolongation of AV nodal conduction time and caused typical Wenckebach AV block in all 16 patients with EC 50 and E max values of 1.4 ± 0.8 mg and 54 ± 2%, respectively. Adenosine also induced dose-dependent prolongation of VA conduction time and VA block, however, with significantly (P &lt; 0.051 higher EC 50 and shorter E max , i.e., 6.1 ± 1 mg and 20 ± 2%, respectively. The mean dose of adenosine to induce AV block is significantly lower than that to induce VA block (3.3 ± 1.6vs. 7.7 ± 3.3 mg, P &lt; 005). Notably, adenosine induced Wenckebach VA block in 10 of 16 patients and Mobitz type II block in 6 of 16 patients. In conclusion, adenosine is more potent in slowing AV than VA conduction, suggesting that the electrical wavefront entering the N zone of AV node is less affected by adenosine during VA than during AV conduction. In addition, retrograde fast pathway may at least in part involve conduction through the N zone of AV node.

1009-50 Pseudo Atrioventricular and Ventriculoatrial Block Induced by Radiofrequency Ablation of Several Atrio-AV Nodal Connections

We determined the roles of the various atrial(A)-atrioventricular nodal (AVN) connections in AV and VA conduction by sequential radiofrequency (RF) ablation. In prior studies, RF ablation applied epicardially to the “fast” pathway (FP) induced A-His bundle (Hb) area delay ≥40 msec and the shift of retrograde A activation from the Hb area to the area of the coronary sinus (CS) ostium, “slow” pathway (SP). Subsequent SP ablation significantly increased the A-H interval, ≥70 msec, and caused VA block in &gt;50%. Histology showed an intact AVN and ablation of its posterior input. In this study, 6 dogs, FP and SP were ablated by the same epicardial approach. Complete AV and VA block were observed in only 1 of 6 dogs. In another 9 dogs, a third lesion was placed endocardially from the fossa ovalis to the entrance of the inferior vena cava, in addition to FP and SP ablation, causing complete AV and VA block in 5 of 9 dogs. During block, a stable AV junctional escape rate (58 ± 10/min) appeared, indicating a supra-hisian pacemaker. In 1 case of “AV block”, pacing from the A close to the Hb showed 1: 1 A-Hb-V conduction up to a rate of 200/min. In addition, there was 1: 1 retrograde conduction to the high right (HR) A with marked conduction delay. In 2 other cases, there was 1: 1 V-HbA conduction during RV pacing, but HRA and CSA electrograms were dissociated. Postmortem, the AV junction showed that all radiofrequency lesions bordered the triangle of Koch. We conclude that there are multiple atrio-AVN connections which provide back-up mechanisms to prevent combined AV and VA block in the normal heart. Moreover, ablation of two or more A inputs can result in pseudo AV and VA block, since some A remains connected to a functional AVN and Hb.

Analysis of junctional ectopy during radiofrequency ablation of the slow pathway in patients with atrioventricular nodal reentrant tachycardia.

Junctional ectopy may occur during radiofrequency (RF) catheter ablation of the slow pathway in patients with atrioventricular nodal reentrant tachycardia (AVNRT). The purpose of the present study was to characterize this junctional ectopy quantitatively. The subjects of this study were 52 consecutive patients with AVNRT who underwent slow pathway ablation and 5 additional patients included retrospectively because they had developed high-degree atrioventricular (AV) block during the procedure. A combined anatomic and electrogram mapping approach was used for slow pathway ablation, and AVNRT was successfully eliminated in all patients. In the group of 52 consecutive patients, the incidence of junctional ectopy was significantly higher during 52 effective applications of RF energy than during 366 ineffective applications (100% versus 65%, P < .001). Compared with ineffective RF energy applications, successful RF energy applications had a significantly longer duration of individual bursts of junctional ectopy (7.1 +/- 7.1 versus 5.0 +/- 7.0 seconds [+/- SD], P < .05), a greater total number of junctional beats during the applications (24 +/- 16 versus 15 +/- 8, P < .01), and a greater total span of time during which junctional ectopy occurred (19 +/- 15 versus 11 +/- 12 seconds, P < .01). Four of the 52 patients plus an additional 5 patients developed transient AV block lasting 34 +/- 37 seconds. In 1 of the 9 patients who had transient AV block, third-degree AV nodal block requiring a permanent pacemaker recurred 2 weeks later. In each of the 9 patients who developed AV block, there was ventriculoatrial (VA) block in association with junctional ectopy during the RF energy application immediately preceding the AV block. Among 48 patients who did not develop AV block, 17 patients had at least one episode of VA block during junctional ectopy. The positive predictive value of VA block during junctional ectopy for the development of AV block was 19% in the consecutive series of 52 patients. Among 31 patients who always had 1:1 VA conduction in association with junctional ectopy, 12 had poor VA conduction in the baseline state, with a VA block cycle length of at least 500 milliseconds during ventricular pacing. In patients with AVNRT undergoing slow pathway ablation, junctional ectopy during the application of RF energy is a sensitive but nonspecific marker of successful ablation. The bursts of junctional ectopy are significantly longer at effective target sites than at ineffective sites. VA conduction should be expected during the junctional ectopy that accompanies slow pathway ablation, even when there is poor VA conduction during baseline ventricular pacing. VA block during junctional ectopy is a harbinger of AV block in patients undergoing RF ablation of the slow pathway. If energy applications are discontinued as soon as VA block occurs, the risk of AV block may be markedly reduced.