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。     

射频消融慢径对房室结双径路患者房室结传导功能的影响

目的 初步探讨房室结双径路是的电生理联系,方法 对３９例（男１３例,女２６例）平均年龄（４６．６±１６．４）岁的房室结哲返性心动过速患进行房室结慢径消融,观察慢径消融对房室结传导功能的影响。结果 成功率１００％,２６例消融后慢径消失（Ⅱ组）１３例消融后慢径残存（Ⅱ组）,消融前后Ｉ组房室结快径前传有效不应期由（３３２．５±４９．５）ｍｓ缩短为（２８２．５±５８．０）ｍｓ前传功能不应期由（３８２．９     

射频消融房室结慢径对房地传导功能的电生理影响

５８例射频消融（ＲＦＣＡ）房室结慢径对房室结传导功能的电生理影响结果ＲＦＣＡ后房室结正向１：１传导的最短周期延长、快径前传有效不应期缩短，慢径前传有效不应期无明显改变，不影响房室结传导功能。     

射频消融慢径后房室结电生理特性变化的探讨

目的:探讨房室结折返性心动过速(AVNRT)患者消融慢径对房室结电生理特性的影响。方法:①比较34例患者射频消融术前及术后AH间期、房室结前传及逆传文氏周期、快径路及慢径路前传有效不应期。②根据术后慢径是否消失将34例患者分为:慢径消失组(n=24);慢径改良组(n=10),比较两组间快径及慢径前传有效不应期。结果:房室结改良前后文氏周期变化:34例患者在未分组前射频消融前后房室结文氏周期无明显变化。快径前传有效不应期:慢径消失组快径前传有效不应期术后较术前降低,有显著性差异(P<0．05);慢径改良组慢径前传有效不应期术后较术前延长,有显著性差异(P<0．05)。结论:快径前传有效不应期的缩短与消融后慢径是否残存有关;慢径的消融影响房室结的前向传导。     

射频消融房室结慢径对快径传导功能的影响（摘要）

射频消融房室结慢径对快径传导功能的影响（摘要）杨新春葛永贵商丽华胡大一房室结慢径（ＳＰ）消融对快径（ＦＰ）前传功能的影响目前存在争议。有人认为ＳＰ消融后ＦＰ前传有效不应期缩短，也有人认为对ＦＰ前传有效不应期无影响或使房室结前传有效不应期延长。笔者分析...     

房室折返性心动过速合并房室结双径现象

目的 分析射频消融术证实的房室帝道（ＡＰ）合并房室结双径（ＤＡＶＮＰ），以了解其电生理特点。方法 以食管心房调博及心内电生理检查，确诊室上速合并房室结双径１２例，并行射频消融枚。结果 ＡＰ合并ＤＡＶＮＰ占ＡＰ的１６．４％（１２／７３），多为陷匿性ＡＰ（１０／１２），其折返途径多为ＡＰ逆传（１０／１２），房室结单一径路前传，房室结快径道不应期及心动过速时ＲＰ’（ＶＡ）与ＲＰ意期，在食道电生理与心内电     

房室结传导的加速性、疲劳性对房室结功能不应期的影响

房室结传导的加速性、疲劳性对心室免于各种类型的室上性心动过速包括心房颤动的影响起决定作用，但对房室结功能不应期（ＡＶＮ－ＦＲＰ）的影响不明。旨在通过对离体兔心施以多种方案电生理刺激以阐明两者的相互关系。实验结果表明：①房室结传导的加速性使ＡＶＮ－ＦＲＰ缩短（Ｂ方案１４６±３．３ｍｓｖｓＡ方案１５９±３．５ｍｓ，Ｐ＜０．０１，ｎ＝６），疲劳性使ＡＶＮ－ＦＲＰ延长（Ｃ方案１８７±４．９ｍｓｖｓＡ方案１５９±３．５ｍｓ，Ｐ＜０．０１，ｎ＝６）；②加速性和疲劳性诱导的ＡＶＮ－ＦＲＰ的变化是在１１房室传导范围内产生的，并在快速频率下达到它的最大效应（１００％频率下，Ｂ方案１５４±６．０ｍｓ、Ｃ方案１８７±８．３ｍｓ分别与Ａ方案１６８±６．９ｍｓ相比，Ｐ均＜０．０１，ｎ＝６）。结论：ＡＶＮ－ＦＲＰ受房室结传导之加速性、疲劳性相互作用的共同影响，ＡＶＮ－ＦＲＰ的变化可以用来反映房室结的传导功能     

射频消融房室结慢径的电生理改变及与复发的关系

目的探讨射频消融房室结慢径后的电生理改变及与复发的关系。方法５２例确诊房室结双径路伴房室结折返性心动过速患者行慢径消融术，术前及术后分别测量房室结文氏点及快径不应期。随访１～３年，观察远期效果。结果５２例中３例复发，４９例无复发者消融前后快径不应期分别为（３１８．５±５０．２）ｍｓ和（２６６．５±２７．２）ｍｓ（Ｐ＜０．０１）。而３例复发者手术前后不应期分别为３０６．６６ｍｓ和３１６．６６ｍｓ，无明显改变。术后慢径消失者，无１例复发，而残存慢径或伴心房回波者复发率分别为１６．６％及２２．２％。结论慢径残存及快径不应期无改变与复发有关。     

射频消融房室结慢径对房室结传导功能的电生理影响

58例射频消融(RFCA)房室结慢径对房室结传导功能的电生理影响 结果 RFCA后房室结正向1:1传导的最短周期延长、快径前传有效不应期缩短,慢径前传有效不应期无明显改变,不影响房室结传导功能。     

房室结快径电生理特性与慢径消融相互作用的临床研究

目的探讨房室结折返性心动过速慢径消融后对快径传导的影响。方法入选慢快型房室结折返性心动过速患者42例,根据首次放电消融后结果进行分组,第一组:慢径消失组:不能再诱发房室结折返性心动过速;第二组,慢径改良组:可见慢径跳跃现象;第三组:慢径残存组,可见慢径跳跃现象,或后可诱发房室结折返性心动过速。比较三组患者消融前后的快径不应期,快径前传时间,快径前传时间差值变化。结果慢径消失组17例(40.5%),慢径改良组14例(33.3%),慢径残存组11例(26.2%)。慢径消失组患者消融前后快径不应期缩短(234.71±13.28vs331.18±21.18,p0.05)差异存在统计学意义,慢径改良组患者消融后快径不应期缩短(245.71±12.22vs323.57±26.49,p0.05)差异有统计学意义,慢径残存组患者消融前后快径不应期无明显变化(264.55±21.62 vs320.91±15.78,p=0.23)。与慢径残存组相比,慢径消失组和慢径改良组传导消融术后快径不应期以及快径前传时间明显缩短,存在统计学差异。结论慢径完全消融后,快径不应期和快径前传时间均明显缩短,提示慢径消融的同时可以改善房室结快径的前向传导功能,这一现象可结合其他指标作为评价房室结折返性心动过速慢径消融效果的参考。     

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

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

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。     

Prolongation of the fast pathway effective refractory period during cryoablation in children: A marker of slow pathway modification

BACKGROUND: The fast pathway effective refractory period (ERP) has been reported to decrease after slow pathway modification with radiofrequency (RF) energy. How the fast pathway ERP changes during the ablation application has not been reported with either RF or cryoenergy. OBJECTIVES: Using the unique features of cryotherapy, this study assesses the short-term changes in fast pathway ERP during cryomodification of the slow pathway and examines whether these changes are a useful marker for successful slow pathway modification in children. METHODS: Nineteen pediatric patients (median age 15.1 years, range 9.6-19.6 years; weight 60.7 kg, range 35.6-130.2 kg) with anterograde dual AV nodal physiology underwent slow pathway modification with catheter-based cryoablation. Programmed stimulation was performed during cryoapplications after reaching -25 degrees C to assess fast pathway and slow pathway conduction. Data were analyzed from 59 of 237 cryoapplications where the fast pathway ERP was measured more than once (n = 13 patients). RESULTS: For 23 of 59 applications where the slow pathway was modified, the fast pathway ERP significantly increased during cryotherapy (Delta = 33.5 ms, P <.0001). The magnitude of fast pathway ERP prolongation during cryotherapy was larger when the slow pathway was modified than when there was no effect on slow pathway conduction (33.5 +/- 30.5 vs 5.8 +/- 18.9 ms, P =.0005). Prolongation of fast pathway ERP by >/=20 ms had 70% sensitivity and 72% specificity for predicting slow pathway modification. Following termination of cryoapplications, which resulted in slow pathway modification, the fast pathway ERP had significantly decreased from baseline (difference 44.5 ms, P <.0001). The effect on fast pathway ERP was not related to changes in cycle length during (R(2) = 0.04, P = .045) or after ablation (R(2) = 0.13, P = .012). CONCLUSION: The fast pathway ERP prolongs during cryoapplications that result in slow pathway modification and shortens after termination of cryoapplications. The magnitude of fast pathway ERP prolongation during cryoapplication may be useful as a marker for successful slow pathway modification.     

Role of the compact node and its posterior extension in normal atrioventricular nodal conduction, refractory, and dual pathway properties

INTRODUCTION: The functional origin of AV nodal conduction, refractory, and dual pathway properties remains debated. The hypothesis that normal conduction and refractory properties of the compact node and its posterior nodal extension (PNE) play a critical role in the slow and the fast pathway, respectively, is tested with ablation lesions targeting these structures. METHODS AND RESULTS: A premature atrial stimulation protocol was performed before and after PNE ablation in six isolated rabbit heart preparations. Discrete (approximately 300 microm) histologically controlled PNE lesions amputated the AV nodal recovery curve from its left steep portion reflecting slow pathway conduction and prevented reentry without affecting the right smooth fast pathway portion of the curve. The ablation shortened A2H2max from 159 +/- 16 ms to 123 +/- 11 msec (P < 0.01) and prolonged the effective refractory period from 104 +/- 6 msec to 119 +/- 11 msec (P < 0.01) without affecting A2H2min (55 +/- 9 msec vs 55 +/- 8 msec; P = NS) and functional refractory period (174 +/- 7 msec vs 175 +/- 6 msec; P = NS). These results did not vary with the input reference used. In six other preparations, lesions applied to the compact node after PNE ablation shifted the fast pathway portion of the recovery curve to longer conduction times and prolonged the functional refractory period, suggesting a compact node involvement in the fast pathway. CONCLUSION: The normal AV nodal conduction and refractory properties reflect the net result of the interaction between a slow and a fast pathway, which primarily arise from the asymmetric properties of the PNE and compact node, respectively.     

Characteristics of slow pathway conduction after successful AVNRT ablation

Background: AV node slow pathway conduction can persist following successful ablation for AV node reentrant tachycardia (AVNRT). We hypothesized that careful examination of AV nodal conduction curves before and after effective AVNRT ablation in patients with persistent slow pathway conduction could shed light on this apparent paradox.
Methods and Results: Thirty patients (age 40.9 ± 14.3; 8 male) were included. AV node function curves were created based on pre- and postablation atrial extrastimulus testing. Analysis of slow pathway function curves demonstrated significant decrease in AH for any given coupling interval after ablation (mean difference –68.1 [–94.5, –41.7] P < 0.001), graphically indicated by downward displacement of the curve. In addition, mean slow pathway effective refractory period (ERP) increased from 247.9 ± 36.1 msec to 288.6 ± 56.0 msec (P < 0.001); mean maximum AH interval decreased from 361.3 ± 114.2 msec to 306.9 ± 65.2 msec (P = 0.013 ) ; mean difference in minimum and maximum AH interval during slow pathway conduction decreased (from 94.5 ± 75.8 msec to 59.6 ± 46.2 msec (P = 0.016 ). Finally, mean difference between the fast and slow pathway effective refractory periods, the span of coupling intervals over which slow pathway conduction occurred, decreased (from 113.9 ± 61.4 msec to 63.2 ± 41.5 msec, P = 0.001).
Conclusions: Ablation, which successfully eliminates inducible and spontaneous AVNRT in the presence of persistent slow pathway conduction, is associated with significantly altered slow pathway conduction characteristics, indicating the presence of a damaged or different slow pathway after ablation, incapable of sustaining 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.     

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.     

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.     

房室结折返性心动过速患者房室结功能曲线连续性的电生理分析

分析房室结折返性心动过速 (AVNRT)中房室结功能曲线呈连续性者的电生理特点。将AVNRT分为房室结功能曲线连续组 (Ⅰ组 )及房室结功能曲线不连续组 (Ⅱ组 ) ,行慢径消融 ,进行消融前后和组间的电生理比较 ,分析房室结功能曲线呈连续性者的特点。结果 :I组心房程序刺激对AVNRT的诱发率仅 42 % (5 / 12 ) ,低于Ⅱ组的 6 6 %(2 3/ 35 )。Ⅰ组房室结前传有效不应期 (ERP AVN)消融前后无显著变化 (2 18.2± 2 9.3msvs 2 5 3.3± 80 .3ms,P >0 .0 5 ) ;心房程序刺激最长A2 H2 间期 (AHmax)消融前后无显著变化 (2 2 5 .8± 71.8msvs 175 .4± 41.9ms,P >0 .0 5 )。Ⅱ组ERP AVN消融后显著延长 (2 78.9± 5 8.9msvs 2 35 .8± 39.6ms,P <0 .0 5 ) ;AHmax消融后显著缩短 (172 .0± 6 7.1msvs 331.6± 86 .6ms ,P <0 .0 5 ) ;消融后房室结快径前传有效不应期 (ERP FP)显著缩短 (2 78.9± 5 8.9msvs 330 .0±5 5 .3ms,P <0 .0 5 )。消融前Ⅰ组AHmax短于Ⅱ组 (P <0 .0 5 ) ,Ⅰ组心动过速时A2 H2 间期 (AHSVT)与消融前AHmax比较差异无显著性 (P >0 .0 5 ) ;Ⅱ组AHSVT短于消融前AHmax(P <0 .0 5 )。结论 :房室结功能曲线连续性者较难经常规心房程序刺激诱发心动过速 ;慢径消融后曲线“尾巴”消失可作为消融终点的一项指     

Differential Effects of Atropine and Isoproterenol on Inducibility of Atrioventricular Nodal Reentrant Tachycardia

Background: Radiofrequency ablation of the slow pathway in atrioventricular nodal reentrant tachycardia (AVNRT) relies on tachycardia non-inducibility after ablation as success criterion. However, AVNRT is frequently non-inducible at baseline. Thus, autonomic enhancement using either atropine or isoproterenol is frequently used for arrhythmia induction before ablation. Methods: 80 patients (57 women, 23 men, age 50±14 years) undergoing slow pathway ablation for recurrent AVNRT were randomized to receive either 0.01mg/kg atropine or 0.5-1.0g/kg/min isoproterenol before ablation after baseline assessment of AV conduction. The effects of either drug on ante- and retrograde conduction was assessed by measuring sinus cycle length, PR and AH interval, antegrade and retrograde Wenckebach cycle length (WBCL), antegrade effective refractory period (ERP) of slow and fast pathway and maximal stimulus-to-H interval during slow and fast pathway conduction. Results: Inducibility of AVNRT at baseline was not different between patients randomized to atropine (73%) and isoproterenol (58%) but was reduced after atropine (45%) compared to isoproterenol (93%, P<0.001). Of the 28 patients non-inducible at baseline isoproterenol rendered AVNRT inducible in 21, atropine in 4 patients. Dual AV nodal pathway physiology was present in 88% before and 50% after atropine compared to 83% before and 73% after isoproterenol. Whereas both drugs exerted similar effects on ante- and retrograde fast pathway conduction maximal SH interval during slow pathway conduction was significantly shorter after isoproterenol (300±48ms vs. 374±113ms, P=0.012). Conclusion: Isoproterenol yields higher AVNRT inducibility than atropine in patients non-inducible at baseline. This may be caused by a more pronounced effect on antegrade slow pathway conduction.