Pseudo-atrial fibrillation, rare manifestation of multiple anterograde atrioventricular nodal pathways

In patients with dual or multiple atrioventricular (AV) nodal pathways manifesting nonreentrant tachycardia or unusual forms of AV nodal reentry, paroxysmal atrial fibrillation is often misdiagnosed and patients may erroneously be considered for pulmonary vein isolation. Multiple anterograde slow AV nodal pathways, identified by >1 discontinuity in the anterograde AV nodal conduction curve, are not rare in patients with slow-fast AV nodal reentrant tachycardia (AVNRT). However, only 1 slow AV nodal pathway is usually involved in anterograde conduction during tachycardia. It was reported that patients with multiple anterograde slow AV nodal pathways presented with different tachycardia cycle lengths. For the first time, 2 patients with AVNRT in which maintenance of tachycardia was strictly dependent on participation of 3 different anterograde slow AV nodal pathways in an uniquely alternating sequence are reported. In both patients, a single application of radiofrequency energy in the posterior aspect of Koch's triangle eliminated simultaneously all evidence of anterograde slow pathway conduction. These findings implied that functional differences in a determined circuit based on nonuniform anisotropy rather than anatomically distinct pathways form the electrophysiologic basis for this rare variant of AVNRT. In conclusion, particularly in patients with lone atrial fibrillation who are potential candidates for pulmonary vein isolation, careful analysis of the surface electrocardiogram during irregular supraventricular tachycardia and invasive electrophysiologic examination helps identify rare arrhythmia mechanisms that can be cured by slow pathway ablation alone.     

Atypical forms of supraventricular tachycardia due to atrioventricular node reentry in children after radiofrequency modification of slow pathway conduction

Objectives. This study was performed to investigate the prevalence, mechanisms and clinical significance of supraventricular tachycardias inducible in children or adolescents after radiofrequency modification of slow pathway conduction for the treatment of atrioventricular (AV) node reentrant tachycardia.Background. Limited data have been reported with regard to the physiology of AV node reentrant tachycardia in young patients. Radiofrequency catheter ablation allows evaluation of the effects of selective modification of the different pathways involved in AV node reentrant tachycardia.Methods. Selective modification of slow pathway conduction was performed in 18 young patients (12.9 ± 3.4 years old) with typical (anterograde slow-retrograde fast) AV node reentrant tachycardia. Radiofrequency energy was applied across the posteromedial or midseptal tricuspid annulus, guided by slow pathway potentials and anatomic position. Programmed stimulation was performed after modification of slow pathway conduction defined as noninducibility of typical AV node reentrant tachycardia.Results. Modification of slow pathway conduction was achieved in each patient, with a median of four applications of radiofrequency energy. However, atypical forms of supraventricular tachycardia were inducible in 9 of 18 young patients after slow pathway modification: AV node reentrant tachycardia with 2 to 1 AV block (seven patients; anterograde fast-retrograde slow AV node reentrant tachycardia (five patients); and sustained accelerated junctional tachycardia (two patients). In comparison, atypical forms of tachycardia were inducible in only 2 of 59 adult patients with AV node reentrant tachycardia undergoing slow pathway modification in the same laboratory (p = 0.01). Additional applications of radiofrequency energy to the posteromedial tricuspid annulus rendered AV node reentrant tachycardia with 2 to 1 block and the fast-slow form of AV node reentrant tachycardia noninducible. Junctional tachycardia terminated spontaneously in both patients. During 9.8 ± 3 months of follow-up, slow-fast AV node reentrant tachycardia has recurred in one patient, whereas fast-slow AV node reentrant tachycardia has occurred in two patients, both with inducible fast-slow tachycardia after the initial modification of slow pathway conduction.Conclusions. Initial applications of radiofrequency energy may selectively modify the anterograde conduction of slow pathway fibers in young patients with AV node reentrant tachycardia. This may result in AV node reentrant tachycardia with 2 to 1 AV block or a reversal of the reentrant circuit (fast-slow tachycardia). Induction of these tachyarrhythmias indicates that further applications of radiofrequency energy are required for the successful modification of slow pathway conduction in young patients. The increased prevalence of inducible atypical arrhythmias among young patients suggests differences in the anatomic or electrophysiologic substrate of AV node reentrant tachycardia that may evolve as a function of age.     

Slow pathway ablation in patients with atrioventricular node reentrant tachycardia and a prolonged PR interval

Objectives. We sought to assess the safety and efficacy of selective slow pathway ablation using radiofrequency energy and a transcatheter technique in patients with a prolonged PR interval and atrioventricular (AV) node reentrant tachycardia.Background. Although both fast and slow AV node pathways can be ablated in patients with AV node reentrant tachycardia, slow pathway ablation, by obviating the risk of AV block, appears to be safer. However, the safety and efficacy of selective slow pathway ablation using transcatheter radiofrequency energy in patients with a prolonged PR interval during sinus rhythm are unclear.Methods. The seven study patients with a prolonged PR interval (mean ± SD 237 ± 26 ms) comprised three women and four men with a mean age of 31 ± 15 years. The slow pathway was targeted in all seven patients at the posterior/inferior interatrial septal aspect of the tricuspid annulus. Two patients presented with the uncommon variety of AV node reentrant tachycardia after initial fast pathway ablation; in the remaining five patients, the AV node reentrant tachycardia was of the common variety.Results. A single radiofrequency pulse at 30 W successfully abolished the slow pathway in both the anterograde and the retrograde direction in the two patients with uncommon AV node reentrant tachycardia. A mean of 5 ± 3 radiofrequency pulses were required in the remaining five patients with reentrant tachycardia of the common variety. The postablation PR interval and AH interval remained unchanged. The shortest cycle length of 1:1 AV conduction was prolonged significantly (from 327 ± 31 to 440 ± 59 ms, p < 0.01, as was the AV node effective refractory period (from 244 ± 35 to 344 ± 43 ms, p < 0.01). During a mean follow-up interval of 20 ± 6 months, no patient developed symptoms suggestive of AV node reentrant tachycardia or had evidence of second- or third-degree AV block.Conclusions. These data suggest that the AV node slow pathway can be ablated in patients with AV node reentrant tachycardia who demonstrate a prolonged PR interval during sinus rhythm.     

Transcatheter modification of the atrioventricular node using radiofrequency energy.

120 consecutive patients with symptomatic atrioventricular nodal reentrant tachycardia (AVNRT) underwent catheter ablation using radiofrequency energy. Fast pathway ablation was attempted in the first 16 consecutive patients by application of radiofrequency current in the anterior and superior aspect of the tricuspid annulus. Successful results were accomplished in 13 patients, complete AV block occurred in three. The other 104 patients initially underwent ablation of the slow pathway in the posterior and inferior aspects of the tricuspid annulus which was successful in 98 patients. The remaining six patients subsequently underwent a fast pathway ablation with successful results in four and AV block in two. Therefore, 102 (98%) of the last 104 patients became free of AVNRT while maintaining intact AV conduction. This study demonstrates that both AV nodal conduction pathways can be selectively ablated. However, slow pathway ablation seems safer and should be considered as the first approach.     

特殊类型房室结折返性心动过速的电生理机制及其射频消融

报道２例特殊类型的房室结折返性心动过速（ＡＶＮＲＴ），１例为慢－慢型ＡＶＮＲＴ伴起始部多径路逆传；１例为两种不同电生理特性的慢径交替前传、快径逆传构成的ＡＶＮＲＴ。电生理检查均提示房室结三径路。２例病人均于冠状静脉窦口上方消融慢径改良房室结成功，心动过速不再被诱发。随访２个月心动过速均无复发。提示房室结多径路形成的特殊类型ＡＶＮＲＴ，需详细的电生理检查并仔细鉴别方能予以诊断。射频导管消融方法同典型ＡＶＮ－ＲＴ，且安全、有效。     

PR/RR Interval Ratio During Rapid Atrial Pacing:

Method for Confirming Slow Pathway Conduction. Introduction: Although the AV conduction curve in patients with AV nodal reentrant tachycardia (AVNRT) is usually discontinuous, many patients with this arrhythmia do not demonstrate criteria for dual AV nodal pathways. During rapid atrial pacing, the PR interval often exceeds the pacing cycle length when there is anterograde conduction over the slow pathway and AVNRT is induced. The purpose of this prospective study was to determine the diagnostic value of the ratio of the PR interval to the RR interval during rapid atrial pacing as an indicator of anterograde slow pathway conduction in patients undergoing electrophysioiogic testing. Methods and Results: The PR and RR intervals were measured during rapid atrial pacing at the maximum rate with consistent 1:1 AV conduction in four study groups: (1) patients with inducible AV nodal reentry and the classical criterion for dual AV nodal pathways during atrial extrastimulus testing (AVNRT Group 1); (2) patients with inducible AV nodal reentry without dual AV nodal pathways (AVNRT Group 2); (3) control subjects ≤ 60 years of age without inducible AV nodal reentry; and (4) control subjects > 60 years of age without inducible AV nodal reentry. For both groups of patients with inducible AV nodal reentry, AV conduction was assessed before and after radiofrequency ablation of the slow AV nodal pathway. Before slow pathway ablation, the PR/RR ratio exceeded 1.0 in 12 of 13 AVNRT Group 1 patients (mean 1.27 ± 0.21) and 16 of 17 AVNRT Group 2 patients (mean 1.18 ± 0.15, P = NS Group 1 vs Group 2). After slow pathway ablation, the maximum PR/RR ratio was < 1.0 in all AVNRT patients (Group 1 = 0.59 ± 0.08, P < 0. 00001 vs before ablation: Group 2 = 0.67 ± 0.11; P < 0.00001 vs before ablation). Among both groups of control subjects, the PR/RR ratio was > 1.0 in only 3 of 27 patients with no relation to patient age. Conclusion: The ratio of the PR interval to the RR interval during rapid atrial pacing at the maximum rate with consistent 1:1 AV conduction provides a simple and clinically useful method for determining the presence of slow AV nodal pathway conduction. This finding may be particularly useful in patients with inducible AV nodal reentry without dual AV nodal physiology on atrial extrastimulus testing.     

Simultaneous antegrade dual AV node conduction initiates AV nodal re-entrant tachycardia (a rare initiation mechanism)

Typical atrioventricular nodal reentrant tachycardia (AVNRT) is the most common paroxysmal supraventricular tachycardia among adults. The concept of dual pathway physiology remains widely accepted, although this physiology likely results from the functional properties of anisotropic tissue within the triangle of Koch, rather than anatomically distinct tracts of conduction. AVNRT is typically induced with anterograde block over the fast pathway and conduction over the slow pathway, with subsequent retrograde conduction over the fast pathway. On rare occasions, anterograde AV node conduction occurs simultaneously through fast and slow pathways resulting in two ventricular beats in response to one atrial beat. We report a case of AVNRT where the tachycardia is always induced by the same mechanism described above. Successful ablation was achieved by slow pathway modification.     

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.     

Electrophysiological mechanisms of conversion of typical to atypical atrioventricular nodal reentrant tachycardia occurring after radiofrequency catheter ablation of the slow pathway

This report presents an adult patient with conversion of typical to atypical atrioventricular nodal reentrant tachycardia (AVNRT) after slow pathway ablation. Application of radiofrequency energy (3 times) in the posteroseptal region changed the pattern of the atrioventricular (AV) node conduction curve from discontinuous to continuous, but did not change the continuous retrograde conduction curve. After ablation of the slow pathway, atrial extrastimulation induced atypical AVNRT. During tachycardia, the earliest atrial activation site changed from the His bundle region to the coronary sinus ostium. One additional radiofrequency current applied 5 mm upward from the initial ablation site made atypical AVNRT noninducible. These findings suggest that the mechanism of atypical AVNRT after slow pathway ablation is antegrade fast pathway conduction along with retrograde conduction through another slow pathway connected with the ablated antegrade slow pathway at a distal site. The loss of concealed conduction over the antegrade slow pathway may play an important role in the initiation of atypical AVNRT after slow pathway ablation.     

Atrioventricular Nodal Reentry Tachycardia in Patients with Sinus Node Dysfunction: Electrophysiologic Characteristics, Clinical Presentation, and Results of Slow Pathway Ablation

AVNRT and Sinus Node Dysfunction. Introduction: Sinus node dysfunction (SND) is frequently associated with impaired AV conduction. This study investigated the electrophysiologic properties of dual AV nodal pathways in patients suffering from both SND and AV nodal reentrant tachycardia (AVNRT). Methods and Results: Two groups of patients with slow-fast AVNRT underwent invasive electrophysiologic testing and catheter ablation of the slow pathway. Group A comprised 10 patients with SND (age 70 ± 8 years), (Group B included 10 age-matched patients without SND (age 69 ± 7 years; P = NS) who served as controls. Patients of group A exhibited prolongation of the anterograde Wenckebach cycle lengths (WBCLs) of both the fast pathway (559 ± 96 vs 361 ± 38 msec; P < 0.01) and the slow pathway (409 ± 57 vs 339 ± 32 ms; P < 0.01). However, the delta between the WBCLs of the fast and the slow pathways was larger in patients of group A (150 ± 80 vs 22 ± 20 msec; P < 0.01). Retrograde fast pathway conduction was well preserved with no difference in WBCLs (356 ± 42 vs 330 ± 47 msec; P = NS). Cycle lengths of AVNRT were longer in group A (468 ± 46 vs 363 ± 37 msec; P < 0.01). Clinically, all patients of group A suffered from multiple episodes of AVNRT per week, which was not the case in any patient of group B (P < 0.01). Catheter ablation of the slow pathway eliminated AVNRT in all patients without complications. Conclusions: Patients with AVNRT and SND exhibit characteristic electrophysiologic alterations of both AV nodal pathways. Clinically, this results in significantly more frequent episodes of tachycardia. Slow pathway ablation appears to be safe and effective in these patients.     

Selective transcatheter ablation of the fast and slow pathways using radiofrequency energy in patients with atrioventricular nodal reentrant tachycardia.

BACKGROUND. The safety and efficacy of selective fast versus slow pathway ablation using radiofrequency energy and a transcatheter technique in patients with atrioventricular nodal reentrant tachycardia (AVNRT) were evaluated. METHODS AND RESULTS. Forty-nine consecutive patients with symptomatic AVNRT were included. There were 37 women and 12 men (mean age, 43 +/- 20 years). The first 16 patients underwent a fast pathway ablation with radiofrequency current applied in the anterior/superior aspect of the tricuspid annulus. The remaining 33 patients initially had their slow pathway targeted at the posterior/inferior aspect of the right interatrial septum. The fast pathway was successfully ablated in the initial 16 patients and in three additional patients after an unsuccessful slow pathway ablation. A mean of 10 +/- 8 radiofrequency pulses were delivered; the last (successful) pulse was at a power of 24 +/- 7 W for a duration of 22 +/- 15 seconds. Four of these 19 patients developed complete atrioventricular (AV) block. In the remaining 15 patients, the post-ablation atrio-His intervals prolonged from 89 +/- 30 to 138 +/- 43 msec (p less than 0.001), whereas the shortest 1:1 AV conduction and effective refractory period of the AV node remained unchanged. Ten patients lost their ventriculoatrial (VA) conduction, and the other five had a significant prolongation of the shortest cycle length of 1:1 VA conduction (280 +/- 35 versus 468 +/- 30 msec, p less than 0.0001). Slow pathway ablation was attempted initially in 33 patients and in another two who developed uncommon AVNRT after successful fast pathway ablation. Of these 35 patients, 32 had no AVNRT inducible after 6 +/- 4 radiofrequency pulses with the last (successful) pulse given at a power of 36 +/- 12 W for a duration of 35 +/- 15 seconds. After successful slow pathway ablation, the shortest cycle length of 1:1 AV conduction prolonged from 295 +/- 44 to 332 +/- 66 msec (p less than 0.0005), the AV nodal effective refractory period increased from 232 +/- 36 to 281 +/- 61 msec (p less than 0.0001), and the atrio-His interval as well as the shortest cycle length of 1:1 VA conduction remained unchanged. No patients developed AV block. Among the last 33 patients who underwent a slow pathway ablation as the initial attempt and a fast pathway ablation only when the former failed, 32 (97%) had successful AVNRT abolition with intact AV conduction. During a mean follow-up of 6.5 +/- 3.0 months, none of the 49 patients had recurrent tachycardia. Forty patients had repeat electrophysiological studies 4-8 weeks after their successful ablation, and AVNRT could not be induced in 39 patients. CONCLUSIONS. These data suggest that both fast and slow pathways can be selectively ablated for control of AVNRT. Slow pathway ablation, however, by obviating the risk of AV block, appears to be safer and should be considered as the first approach.     

Transient entrainment and interruption of atrioventricular node tachycardia

The possibility of transiently entraining and interrupting the common type of atrioventricular (AV) node tachycardia (anterograde slow, retrograde fast AV node pathway) was studied using atrial and ventricular pacing in 18 patients with paroxysmal AV node tachycardia. Transient entrainment occurred in all patients. During atrial pacing, localized block in the AV node for one beat followed by anterograde conduction over the fast pathway was observed in three patients. During ventricular pacing, localized block for one beat followed by retrograde conduction over the slow pathway was not observed in any patient. Neither atrial nor ventricular fusion beats were observed during entrainment. These observations indicate in a way not previously shown that reentry involving two functionally dissociated pathways in the AV node is the underlying mechanism of paroxysmal AV node tachycardia. The inability to demonstrate atrial or ventricular fusion beats during entrainment suggests a true intranodal location of the reentrant circuit. Finally, the ability to transiently entrain intranodal tachycardia demonstrates that this electrophysiologic phenomenon is not exclusively limited to macroreentrant circuits.     

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.     

房室结折返性心动过速慢径消融终点与复发的关系

目的:观察房室结折返性心动过速(AVNRT)的慢径消融终点与复发的联系。方法:534个慢-快型AVNRT患者行慢径消融治疗,观察A型终点(彻底消融慢径,房室结无跳无折)和B型终点(残留慢径有或无1～3心房回波,不能诱发AVNRT)与AVNRT复发的联系及对房室结传导的影响。结果:①A型复发5例(1.2%),B型复发11例(9.4%),差异有统计学意义(P0.05)。②A型终点房室结前传文氏周期(Wen-AVN)、快径前传有效不应期和房室结双径路(DAVNP)的跳跃增值缩短,B型快径前传有效不应期和房室结双径路的跳跃增值缩短,A型有效不应期的缩短明显大于B型。结论:A型终点的复发率明显低于B型终点;只要改变房室传导功能,不能诱发心动过速,B型终点仍然是有效、可靠的消融终点。     

Incessant nonreentrant atrioventricular nodal tachycardia due to multiple nodal pathways treated by radiofrequency ablation of the slow pathways

In patients with dual AV nodal physiology, simultaneous anterograde fast and slow pathway conduction resulting in an unusual form of nonreentrant AV nodal tachycardia has been observed. We describe the case of a young patient with an incessant form of complex supraventricular tachycardia who underwent electrophysiologic evaluation, which showed simultaneous conduction via multiple AV nodal pathways that caused a unique form of incessant nonreentrant AV nodal tachycardia. Radiofrequency ablation of the spatially closed intermediate and slow pathways effectively treated the tachycardia. The electrophysiologic determinants of simultaneous conduction through the multiple nodal pathways and the apparently different behavior of the fast pathway before and after ablation are discussed.     

Nature of dual atrioventricular node pathways and the tachycardia circuit as defined by radiofrequency ablation technique.

OBJECTIVES. A comprehensive electrophysiologic study followed by selective radiofrequency ablation from three sites was performed in patients with atrioventricular (AV) node reentrant tachycardia to better delineate the nature of the tachycardia circuit. BACKGROUND. We postulated that the retrograde fast pathway is the anterior superficial group of transitional cells and the slow pathway is the compact node with its posterior input of transitional cells. Twenty-three consecutive patients were studied. In nine, the atria could be dissociated from the tachycardia by delivery of an atrial extrastimulus during tachycardia. METHODS. Radiofrequency ablation was performed with three approaches. The anterior approach was designed to interrupt the anterior superficial atrial input to the compact node, the posterior approach to interrupt the posterior atrial input to the compact node and the inferior approach to destroy the compact node itself. RESULTS. Selective ablation of the retrograde fast pathway was achieved in seven patients, six with the anterior and one with the inferior approach. Anterograde fast pathway conduction was not affected, whereas retrograde fast pathway conduction was either abolished or markedly depressed. None had induction of echoes or tachycardia after ablation. Selective ablation of the slow pathway was successful in 13 patients, 1 with anterior, 3 with posterior and 9 with inferior approaches. In these 13 patients, both anterograde and retrograde fast pathway conduction were not affected, the dual pathway physiology was abolished and the tachycardia was not inducible after ablation. Ablation of both the retrograde fast pathway and the slow pathway occurred with the inferior approach in three patients. CONCLUSIONS. We conclude that the retrograde fast pathway is likely to be the anterior superficial group of transitional cells, whereas the slow pathway is the compact node and its posterior input of transitional cells. A barrier seems to exist between the atrium and the tachycardia circuit. In a broad view of the AV node structure, the tachycardia circuit is confined to the node.     

Patient with atrioventricular node reentrant tachycardia with eccentric retrograde left-sided activation: treatment with radiofrequency catheter ablation

We describe a patient with supraventricular tachycardia with triple atrioventricular (AV) node pathway physiology. A discontinuous curve was present in the antegrade AV nodal function curves. During right ventricular pacing, the earliest retrograde atrial activation was recorded at the left-sided coronary sinus electrode. The retrograde ventricular-atrial interval was long and had decremental conduction. We induced a slow-slow AV node reentrant tachycardia (AVNRT) with eccentric retrograde left-sided activation. After slow pathway ablation, dual AV nodal pathway physiology was present. AVNRT with eccentric retrograde left-sided activation is relatively rare, and our findings suggest that eccentric retrograde left-sided atrial inputs consist partially of a slow pathway and disappear with slow pathway ablation.     

Elimination of atrioventricular nodal reentrant tachycardia using discrete slow potentials to guide application of radiofrequency energy.

BACKGROUND. Ablation of the slow pathway has been performed to eliminate atrioventricular (AV) nodal reentrant tachycardia (AVNRT) either by a surgical approach or by using radiofrequency catheter technique guided by retrograde slow pathway activation mapping. From previous experience of midseptal and posteroseptal mapping, we were aware of the existence of peculiar slow potentials in most humans. Postulating their role in AVNRT, we studied these potentials and the effects of radiofrequency energy. METHODS AND RESULTS. Sixty-four patients (mean age, 48 +/- 19 years) with the usual form of AVNRT were studied. Slow, low-amplitude potentials were recorded when using the anterograde AV conducting system. Slow potentials occupied all (giving a continuum of electrograms) or some of the time between the atrial and ventricular electrograms. Their most specific patterns were their progressive response to increasing atrial rates, which resulted in a dramatic decline in amplitude and slope, a corresponding increase in duration, and a separation from preceding atrial potentials until the disappearance of any consistent activity. Slow potentials were recorded along a vertical band at the mid or posterior part of the septum near the tricuspid annulus. Radiofrequency energy applied at the slow potential site resulted in interruption of induced tachycardia within a few seconds and rendered tachycardia noninducible in all patients. A median of two impulses was delivered to each patient. In 69% of patients, postablation atrial stimulation cannot achieve a long atrial-His interval, which previously was critical for tachycardia induction or maintenance. No patient had AVNRT over a follow-up period of 1-16 months, and all had preserved AV conduction. In all except two patients, the PR interval was unchanged. In 47 patients, long-term electrophysiological studies confirmed the efficacy of ablation and the nonreversibility of results by isoproterenol; however, echo beats remained inducible in 40% of patients. CONCLUSIONS. An area showing slow potentials is present at the perinodal region in humans. In patients with AVNRT, application of radiofrequency energy renders tachycardia noninducible through the preferential modification of the anterograde slow pathway. With present clinical methods, the exact origin and significance of these physiological potentials cannot be specified.     

下位法射频消融慢径路改良房室结治疗室上性心动过速23例

用下位法射频消融慢径路改良房室结治疗房室结折返性心动过速(AVNRT)18例,房室折返性心动过速(AVRT)5例.AVNRT中16例为慢—快型,1例快—慢型,1例慢—快型与快—慢型并存,18例慢径路全部阻断成功.AVRT中1例显性预激,4例隐性预激,有5例慢径路和3例房室旁路消融成功.射频放电时21例出现结性心律.无严重并发症出现.AVNRT病人中随仿1—15个月有1例复发,第二次射频成功.认为下位法射频消融阻断慢径路成功率高,并发症少.     

Role of compact node and posterior extension in direction-dependent changes in atrioventricular nodal function in rabbit

INTRODUCTION: AV nodal conduction properties differ in the anterograde versus the retrograde direction. The underlying substrate remains unclear. We propose that direction-dependent changes in AV nodal function are the net result of those occurring in the slow and fast pathways. METHODS AND RESULTS: Anterograde and retrograde AV nodal properties were determined with a premature protocol before and after posterior extension (slow pathway) ablation, and before and after upper compact node (fast pathway) ablation. Each ablation was performed in a different group of six rabbit heart preparations. In control, nodal minimum conduction time (NCTmin) and effective refractory period (ERPN) typically were longer, and maximum conduction time (NCTmax) was shorter in the retrograde compared to the anterograde direction. Posterior extension ablation prolonged anterograde ERPN from 91 +/- 10 ms to 141 +/- 15 ms (P < 0.01) and shortened NCTmax from 150 +/- 13 ms to 82 +/- 7 ms (P < 0.01) but did not affect retrograde conduction. Thus, the posterior extension normally contributes to the anterograde but not retrograde recovery curve. Compact node ablation prolonged anterograde conduction (NCTmin increased from 57 +/- 2 ms to 73 +/- 7 ms, P < 0.01) but did not alter ERPN and NCTmax. This ablation abolished retrograde conduction in two preparations and resulted in retrograde slow pathway conduction in four, the latter being interrupted by posterior extension ablation. Thus, the compact node accounts for the baseline of the recovery curve in both directions. Ablation of the compact node results in anterograde slow pathway conduction over the entire cycle length range and may result in retrograde slow pathway conduction. CONCLUSION: Direction-dependent properties of the AV node arise from those of the compact node-based fast pathway and posterior extension-based slow pathway. Normal AV node has bidirectional dual pathways.