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.     

Noninvasive diagnosis of dual AV nodal physiology in patients with AV nodal reentrant tachycardia by adenosine triphosphate test

Atrioventricular nodal reentrant tachycardia (AVNRT) is a relatively common paroxysmal supraventricular tachycardia. This study investigated whether adenosine-5'-triphosphate (ATP) injection during sinus rhythm might be useful in the noninvasive diagnosis of dual AV nodal pathways. The study group consisted of 9 patients with slow/fast AVNRT and 11 control patients without antegrade dual AV nodal physiology (DAVNP). ATP (2.5 to 30 mg, in 2.5-mg increments was injected during sinus rhythm until signs of DAVNP (> or = 50 msec increase or decrease in AH or PR interval in two consecutive beats) or > or = second-degree AV block was observed. DAVNP was diagnosed by ATP test in all 9 patients with slow/fast AVNRT. DAVNP was observed by ATP test in 3 of the 11 control patients. Thus, the test had a sensitivity of 100% and specificity of 73%. ATP test given during sinus rhythm is useful for identifying patients with dual AV nodal pathways who are prone to AVNRT.     

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.     

从慢慢型和慢快型房室结折返性心动过速电生理特性的差异分析折返环的不同

目的从慢慢型房室结折返性心动过速（AVNRT）和慢快型AVNRT的电生理特性的差异分析两型AVNRT间折返环的不同.方法在500例AVNRT患者中的59例慢慢型和60例慢快型之间,比较部分电生理特性的异同;同时在部分慢慢型和慢快型患者中应用2种方法（1）比较起搏时和心动过速时的HA间期的长度;（2）比较心动过速时心室刺激重整心动过速的不同.比较下传共径（LCP）的异同.结果慢慢型的前传慢径和逆传慢径有明显不同的传导时间;慢慢型的逆传慢径与慢快型的逆传快径有明显不同的传导时间和递减特性;和慢快型相比,2种方法均显示慢慢型有较长的LCP.结论 （1）慢慢型AVNRT中前传慢径和逆传慢径的传导时间明显不同;慢慢型较慢快型有较长的下传共径;（2）研究结果支持慢慢型AVNRT可能应用房室结的右侧后延伸和左侧后延伸分别形成心动过速的前传和逆传支而形成折返.     

Differential Effect of Esmolol on the Fast and Slow AV Nodal Pathways in Patients with AV Nodal Reentrant Tachycardia

Esmolol Effect on AV Nodal Pathways. Introduction: AV nodal reentrant tachycardia (AVNRT) usually involves anterograde conduction over a slowly conducting (“slow”) pathway and retrograde conduction over a rapidly conducting (“fast”) pathway. A variety of drugs, such as beta blockers, digitalis, and calcium channel blockers, have been reported to prolong AV nodal refractoriness in both the anterograde and retrograde limbs of the circuit. However, few data are available that address whether the fast and slow pathways respond in a quantitatively different manner to drugs such as beta-adrenergic antagonists. In addition, it is not known whether the effects of these agents on refractoriness parallel the effects on conduction in the fast and slow pathways. The present study was performed to measure the effect of the intravenous beta-adrenergic agent, esmolol, on refractoriness and conduction in both the fast and slow AV nodal pathways in patients with AVNRT. Methods and Results: Thirteen patients with discontinuous AV nodal conduction properties and typical AVNRT were studied. Anterograde and retrograde AV nodal functional assessment was performed at baseline and following steady-state drug infusion of intravenous esmolol at a dose of 500 μg/kg for 1 minute, 150 /μg/kg per minute for the next 4 minutes, followed by a continuous maintenance infusion of 50 to 100 μg/kg per minute. The anterograde effective refractory period of the fast pathway increased from 381 ± 75 msec at baseline to 453 ± 92 msec during the infusion of esmolol (P = 0.003). The anterograde effective refractory period of the slow pathway was also prolonged by esmolol, from 289 ± 26 msec to 310 ± 17 msec (P = 0.005). However, the absolute magnitude of the change in the anterograde effective refractory period of the fast pathway (+72 ± 59 msec) was significantly greater than the change in anterograde effective refractory period of the slow pathway (+21 ± 16 msec, P = 0.01). The mean retrograde effective refractory period of the fast pathway increased from 276 ± 46 msec to 376 ± 61 msec during esmolol infusion (P = 0.03). Retrograde slow pathway conduction that could not be demonstrated at baseline became manifest in three patients during esmolol infusion. In contrast to the effects of esmolol on refractoriness, the AH interval during anterograde slow pathway conduction prolonged to a far greater extent (+84 msec) than the HA interval associated with retrograde fast pathway conduction (+5 msec, P = 0.04). Conclusion: The beta-adrenergic antagonist, esmolol, has a quantitatively greater effect on anterograde refractoriness of the fast than the slow AV nodal pathway. However, the effects on conduction intervals during AVNRT are greater in the anterograde slow pathway than in the retrograde fast pathway. These observations suggest that the fast and slow pathways may have differential sensitivities to autonomic influences. This difference in the response to beta-adrenergic antagonists may be exploited as a clinically useful method for demonstrating slow pathway conduction in some individuals with AVNRT.     

Electrophysiologic study demonstrating triple antegrade AV nodal pathways in patients with spontaneous and/or induced supraventricular tachycardia

Ten patients are described with two discrete discontinulties in AV nodal conduction curves suggesting triple antegrade AV nodal pathways. This represents approximately 6% of patients seen in this laboratory with dual AV nodal pathways. Patients ranged in age from 18 to 63 (mean ± Sd, 48 ± 15 years). Six of the 10 patients had organic heart disease and four did not. The effect of cycle length on triple pathways could be analyzed in 8 of 10 patients who had atrial extrastimulus testing at two or more cycle lengths. Three of these eight patients had triple pathways at all tested cycle lengths. Four patients had triple pathways only at shorter cycle lengths. One patient had triple pathways only at longer cycle lengths. Intact retrograde conduction was demonstrated in seven of ten patients, all of whom had atrial echoes (two patients) or inducible supraventricular tachycardia (SVT) (five patients). Echoes or SVT were induced on the slow pathway is all seven patients, but also on the intermediate pathway in three. However, sustained SVT usually reflected antegrade slow and retrograde fast pathway conduction. In conclusion. triple AV nodal pathways may be demonstrated in occasional patients during atrial extrastimulus testing. Thereby, functional longitudinal dissociation of the AV node is not limited to two pathways.     

Electrophysiologic Spectrum of Atrioventricular Nodal Behavior in Patients with Atrioventricular Nodal Reentrant Tachycardia Undergoing Selective Fast or Slow Pathway Ablation

AV Nodal Behavior After Ablation. Introduction; The objective of this report is to delineate the atrioventricular (AV) nodal electrophysiologic behavior in patients undergoing fast or slow pathway ablation for control of their AV nodal reentrant tachycardia (AVNRT).
Methods and Results: One hundred sixteen consecutive patients with symptomatic AVNRT were included. Twenty-two patients underwent fast pathway ablation with complete abolition of AVNRT in all and development of complete AV block in five patients. Of 17 patients with intact AV conduction postablation, 12 had demonstrated antegrade dual pathway physiology during baseline study, which was maintained in three and lost in nine patients postablation. Two patients with successful fast pathway ablation developed uncommon AVNRT necessitating a slow pathway ablation. Twenty-one patients demonstrated both common and uncommon forms of AV nodal reentry during baseline study. The earliest site of atrial activation was close to the His-bundle recording site (anterior interatrial septum) during common variety and the coronary sinus ostium (posterior interatrial septum) during the uncommon AV nodal reentry in all 21 patients. Ninety-six patients underwent successful slow pathway ablation. Among these, the antegrade dual pathway physiology demonstrable during baseline study (60 patients) was maintained in 25 and lost in 35 patients postablation.
Conclusion: These data suggest that: (1) dual pathway physiology may persist after successful ablation, which might be a reflection of multiple reentrant pathways in patients with AVNRT: and (2) the retrograde pathways during common and uncommon AVNRT have anatomically separate atrial breakthroughs. These findings have important electrophysiologic implications regarding the prevailing concept of the AV nodal physiology in patients with AVNRT.     

The Electrophysiologic Characteristics in Patients with Only Ventricular-Pacing Inducible Slow–Fast Form Atrioventricular Nodal Reentrant Tachycardia

Background: Atrioventricular nodal reentrant tachycardia (AVNRT) can be usually induced by atrial pacing or extrastimulation. However, it is less commonly induced only by ventricular pacing or extrastimulation. Objective: The purpose of this retrospective study was to investigate the electrophysiologic characteristics in patients with slow–fast form AVNRT that could be induced only by ventricular pacing or extrastimulation. Methods: The total population was 1497 patients associated with AVNRT. There were 1373 (91.7%) patients who had slow–fast form AVNRT included in our study. Group 1 (n = 45) could be induced only by ventricular pacing or extrastimulation, and Group 2 (n = 1328) could be induced by only atrial stimulation or both atrial and ventricular stimulation. The electrophysiologic characteristics of the group 1 and group 2 patients were compared. Results: Group 1 patients had a significantly lower incidence of both antegrade and retrograde dual AV nodal pathways. The pacing cycle length (CL) of the antegrade 1:1 fast pathway (FP) and antegrade ERP of the FP were both significantly shorter in Group 1 patients. Mean antegrade FRP of the fast and slow pathways were significantly shorter in Group 1 patients. The differences of pacing CL of 1:1 antegrade conduction, antegrade ERP and FRP were much longer in Group 2 patients. Conclusion: This study demonstrated the patients with slow–fast form AVNRT that could be induced only by ventricular stimulation had a lower incidence of dual AV nodal pathways and the different electrophysiologic characteristics (shorter pacing CL of the antegrade 1:1 FP, antegrade ERP of the FP and the differences of pacing CL of 1:1 antegrade conduction, antegrade ERP and FRP) from the other patients. The specific electrophysiologic characteristics in such patients could be the reason that could be induced only by ventricular stimulation.     

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.     

Multiple AV nodal pathways in patients with AV nodal reentrant tachycardia--more common than expected?

AIMS: It was the purpose of this study to determine the incidence of more than two AV nodal pathways in patients with AVNRT. METHODS AND RESULTS: In 78 consecutive patients with AV-nodal reentrant tachycardias (AVNRT) (50 females, 28 males, mean age 52.8 +/- 14.6 years), the number of sudden AH increases by 50 ms or more (AH-jump) was analysed during atrial extrastimulation. The incidence of two AV nodal pathways was accepted to be present in patients with AVNRT without an AH-jump ('smooth curve'). The following forms of tachycardia were induced: a typical AVNRT (slow-fast) in 67 patients, an atypical AVNRT (fast-slow) in 12 patients and a slow-slow-AVNRT in 4 patients. Five patients had two forms of AVNRT. 47 patients (60.3%) showed two AV nodal pathways, 27 patients (34.6%) had three AV-nodal pathways and 4 patients (5.1%) exhibited four AV-nodal pathways. For successful catheter ablation of AVNRT in patients with more than two pathways, more radiofrequency energy applications were required (9.2 +/- 6.3) compared with patients with only two pathways (6.7 +/- 4.8). Furthermore, in patients with more than two AV-nodal pathways, the catheter intervention resulted more frequently in a modulation of slow pathway conduction than in an ablation of the slow pathway(s). CONCLUSION: The incidence of more than two AV-nodal pathways in patients with AVNRT was unexpectedly high at about 40%. Thus, these tachycardias require a meticulous electrophysiological evaluation for successful ablation.     

New Evidence that AV Node Slow Pathway Conduction Directly Influences Fast Pathway Function

Interaction Between the Slow and Fast Pathway. Introduction: Shortening of the AV node fast pathway effective refractory period (ERP) following successful slow pathway ablation may be a nonspecific effect of energy application at the AV junction or may be due to elimination of a direct effect of slow pathway conduction on the fast pathway.
Methods and Results: Twenty-six consecutive patients (20 women and 6 men; mean age 45 ± 3 years) with typical AV nodal reentrant tachycardia who underwent successful slow pathway ablation (defined as complete elimination of dual AV node physiology) were studied. The fast pathway ERP (at a drive train cycle length of 600 msec) was determined prior to ablation (baseline) and following unsuccessful and successful ablation attempts. Successful slow pathway ablation shortened the fast pathway ERP significantly (317 ± 9 msec; P < 0.001) compared to baseline (386 ± 12 msec), whereas unsuccessful ablations bad no effect (376 ± 11 msec). Sinus cycle length, the AH interval, and blood pressure were unchanged following successful ablation. Shortening of the fast pathway ERP did not correlate with the number of energy applications or with two measures of the proximity between the slow and the fast pathway.
Conclusion: These results support the hypothesis that shortening of the fast pathway ERP following slow pathway ablation is due to elimination of a direct effect of slow pathway conduction on fast pathway function rather than a nonspecific effect of repeated energy delivery at the AV junction.     

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.     

从慢径消融发生的交界区心律试探房室结双径的本质

７６例慢－快型房室结折返性心动过速（ＡＶＮＲＴ）患者接受房室结慢径消融术。６５例慢径阻断、９例双径存在但ＡＶＮＲＴ不能诱发、２例快径阻断。慢径阻断后，除快径的前传有效不应期（ＥＲＰ）缩短（２８７．０±７９．０ｍｓｖｓ３４４．０±８７．０ｍｓ，Ｐ＜０．０１）外，房室传导的文氏点、２１阻滞点、室房传导的１１点、快径逆传ＥＲＰ、前传和逆传功能不应期均无明显改变。共放电８４１次，其中无交界区心律的３１７次放电，无一次消融成功。６５例慢径阻断者，交界区心律减少或消失。以上结果提示快径和慢径可能是两条各具电生理特性的传导纤维。     

Need for Fast Pathway Ablation in Typical Irregular AV Nodal Reentrant Tachycardia in a Patient with Multiple AV Nodal Pathways

A case of a 60-year-old male with irregular AV nodal reentrant tachycardia of the common type is reported. Electrophysiological study revealed multiple antegrade slowly conducting AV nodal pathways and one exclusively retrogradely conducting fast AV nodal pathway. Despite the recommendation for slow pathway ablation as the treatment of choice in patients with AVNRT, first pathway ablation was successfully performed in this case due to the risk of total A V block of ablating the slow pathways. The present report shows that there is the rare patient in whom fast pathway ablation is required for curative treatment of AV nodal reentrant tachycardia.     

Atrioventricular nodal reentrant tachycardia in children: effect of slow pathway ablation on fast pathway function

INTRODUCTION: Prior studies in adults have shown significant shortening of the fast pathway effective refractory period after successful slow pathway ablation. As differences between adults and children exist in other characteristics of AV nodal reentrant tachycardia (AVNRT), we sought to characterize the effect of slow pathway ablation or modification in a multicenter study of pediatric patients. METHODS AND RESULTS: Data from procedures in pediatric patients were gathered retrospectively from five institutions. Entry criteria were age <21 years, typical AVNRT inducible with/without isoproterenol infusion, and attempted slow pathway ablation or modification. Dual AV nodal pathways were defined as those with > or =50 msec jump in A2-H2 with a 10-msec decrease in A1-A2. Successful ablation was defined as elimination of AVNRT inducibility. A total of 159 patients (age 4.4 to 21 years, mean 13.1) were studied and had attempted slow pathway ablation. AVNRT was inducible in the baseline state in 74 (47%) of 159 patients and with isoproterenol in the remainder. Dual AV nodal pathways were noted in 98 (62%) of 159 patients in the baseline state. Ablation was successful in 154 (97%) of 159 patients. In patients with dual AV nodal pathways and successful slow pathway ablation, the mean fast pathway effective refractory period was 343+/-68 msec before ablation and 263+/-64 msec after ablation. Mean decrease in the fast pathway effective refractory period was 81+/-82 msec (P < 0.0001) and was not explained by changes in autonomic tone, as measured by changes in sinus cycle length during the ablation procedure. Electrophysiologic measurements were correlated with age. Fast pathway effective refractory period was related to age both before (P = 0.0044) and after ablation (P < 0.0001). AV block cycle length was related to age both before (P = 0.0005) and after ablation (P < 0.0001). However, in dual AV nodal pathway patients, the magnitude of change in the fast pathway effective refractory period after ablation was not related to age. CONCLUSION: Lack of clear dual AV node physiology is common in pediatric patients with inducible AVNRT (38%). Fast pathway effective refractory period shortens substantially in response to slow pathway ablation. The magnitude of change is large compared with adult reports and is not completely explained by changes in autonomic tone. Prospective studies in children using autonomic blockade are needed.     

从射频消融探讨房室结双径路的本质和房室结改良的机制

采用两种方法对142例房室结折返性心动过速(AVNRT)患者进行房室结改良。128例慢—快型AVNRT中,83例单纯慢径改良,33例慢径前传和快径逆传同时改良,3例单纯快径逆传改良,7例快径前传和慢径或快径逆传同时改良,2例失败。1例发生永久性Ⅲ度房室传导阻滞;10例快—慢型和4例慢—慢型AVNRT患者均慢径改良成功。总成功率98.6％。平均随访6±4月,4例(2.8％)复发,均再次消融成功。慢径改良后,快径前传有效不应期、维持1:1快径前传最短的心房刺激周期明显缩短(P<0.05),而逆向快径有效不应期、维持1:1快径逆传最短的心室刺激周期无明显变化(P>O.05)。本研究提示:快径和慢径可能是解剖上不同的纤维。慢径前传和逆传可以是同一条纤维,也可以是不同的纤维;快径亦然。     

射频消融术中房室结快慢径前传不应期变化及其意义

探讨 2 7例房室结折返性心动过速 (AVNRT)病人射频消融术 (RFCA)中房室结前传有效不应期 (ERP)变化的意义 ,应用心房程序刺激法测定放电前后房室结快慢径前传ERP并据此指导治疗。结果 :2 7例AVNRT病人房室结ERP对射频电流呈 4种反应 :①快径前传ERP缩短 10例。其中 6例表现为引起跳跃的S2 间期缩短 ,无心房回波 ,异丙肾上腺素可诱发AVNRT ,继续寻找并消融慢径 ,跳跃现象消失。 4例前传ERP由 36 0± 15ms缩至 170± 8ms,跳跃消失 ,异丙肾上腺素不能诱发AVNRT ,不再消融。②快径前传ERP延长 6例 ,由 36 0± 10ms增至 430± 12ms。延长S2 与S1耦联间期行心房程序刺激 ,跳跃再现 ,继续寻找并消融慢径至跳跃消失。③慢径前传ERP缩短 5例。术中AVNRT频率由 170± 14次 /分增至 2 30± 11次 /分。继续消融慢径 ,跳跃消失。④慢径前传ERP延长 6例 ,表现为AVNRT的频率减慢 ,继续消融慢径获成功。上述病人经 3.3± 0 .8( 2 .0～ 4.5 )年的随访 ,未见房室阻滞 (AVB)发生 ,亦无AVNRT复发。结论 :对于少数AVNRT病人 ,借助术中房室结前传ERP的变化指导消融 ,可望提高治疗效率、减少复发机率、避免AVB的发生。     

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.     

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.     

Long-term outcome of AV node modulation in 387 consecutive patients with AV nodal reentrant tachycardia

Aim of this study was to assess the long-term results of AV-node modulation in patients with AV nodal reetrant tachycardia. METHODS: From December 1991 until September 1999, AV node modulation (ablation of the fast pathway or ablation/modification of the slow pathway) was performed in 387 consecutive patients with clinically apparent AV nodal reentrant tachycardia. Follow-up data was available in 95% of patients with a mean of 41 +/- 26 months after ablation. RESULTS: Acute success rate was 97%. During long-term follow-up recurrence rate was 7.4% without any difference between fast and slow pathway ablation. Recurrence occurred in 23% of patients with persistent dual AV node physiology after ablation (modification of the slow pathway) in contrast to 3% without dual AV node physiology (ablation of the slow pathway) (p = 0.002). The presence of a dual AV node physiology after slow pathway modulation was the only predictor of recurrence during long-term follow-up. The complication rate was 5.7%. The incidence of complete heart block was 1% without any difference between fast and slow pathway ablation. CONCLUSIONS: Catheter modulation of the AV node for the treatment of AV nodal reentrant tachycardia is effective and safe. During long-term follow-up, the recurrence rate was low. Modulation of the slow pathway is associated with a significantly higher recurrence rate than ablation of the slow pathway.