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.     

经导管射频消融改良房室结治疗房室结折返性心动过速

报道24例病人经射频消融(RFCA)慢径改良房室结治疗房室结折返性心动过速(AVNRT)的研究结果。RFCA后24例病人均不再诱发AVNRT(100％),其中23例慢径传导消失(95.8％),1例慢径传导明显减慢(4.2％)。认为RFCA改良慢径对房室和室房传导没有明显影响,其消融成功的可能预测指标为:X线影象消融电极位于房室结后下部、消融电极图A/V<0.4,放电出现交界性早搏或并行性交界性心律。     

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。     

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。     

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。     

多型房室结折返性心动过速的机制和射频导管消融

目的分析多型房室结折返性心动过速（AVNRT）并存的电生理机制和射频导管消融结果。方法18例经电生理检查后行射频导管消融的多型AVNRT患者。慢快型和慢慢型AVNRT的消融方法为首选消融前传慢径（房室结右侧后延伸）,快慢型AVNRT的消融方法为消融最早慢径逆传心房激动部位。消融成功的标准为消除1：1前传慢径,消除快慢型AVNRT的逆传慢径,不能诱发任何类型AVNRT。结果11例在消融前的电生理检查中诱发出2种类型AVNRT,均在三尖瓣环与冠状静脉窦口之间（房室结右侧后延伸）成功消融。7例在电生理检查中诱发出1种类型,消融此型后又诱发出另外1种类型,其中4例在房室结右侧后延伸进一步消融成功,另3例均经左侧后延伸进一步消融成功。消融术后随访6个月至8年,18例均无复发。结论对于大多数多型AVNRT,房室结右侧后延伸可能为其折返环的主要基质,消融可成功治愈多型AVNRT。在少部分多型AVNRT中,左侧后延伸与右侧后延伸可能分别作为不Ⅻ类型AVNRT折返环的主要基质,需要分别消融才能成功治愈。     

Unusual induction of slow-fast atrioventricular nodal reentrant tachycardia. Report of two cases

INTRODUCTION: Generally, the induction of typical atrioventricular nodal reentrant tachycardia (AVNRT) occurs with a premature atrial stimulus that blocks in the fast pathway and proceeds down the slow pathway slowly enough to allow the refractory fast pathway time to recover. We describe two cases in which a typical AVNRT was induced in an unusual fashion. RESULTS: The first case is a 41-year-old man with paroxysmal supraventricular tachycardia. During the electrophysiology study, the atrial extrastimulus inducing the typical AVNRT was conducted simultaneously over the fast (AH) and the slow pathway (AH'). A successful ablation of the slow pathway was performed. During the follow-up no recurrence was noted. The second case is a 52-year-old woman with a Wolff-Parkinson-White syndrome due to a left posterior accessory pathway. After 5 minutes of atrioventricular reentrant tachycardia (AVRT) induced by a ventricular extrastimulus, a variability of the antegrade conduction was noted in presence of the same VA conduction. In fact, a short AH interval (fast pathway) alternated with a more prolonged AH intervals (slow pathway) that progressively lengthened until a typical AVNRT was induced. The ablation of the accessory pathway eliminated both tachycardias. DISCUSSION: A rare manifestation of dual atrioventricular nodal pathways is a double ventricular response to an atrial impulse that may cause a tachycardia with an atrioventricular conduction of 1:2. In our first case, an atrial extrastimulus was simultaneously conducted over the fast and the slow pathway inducing an AVNRT. This nodal reentry implies two different mechanisms: 1) a retrograde block on the slow pathway impeding the activation of the slow pathway from the impulse coming down the fast pathway, and 2) a critical slowing of conduction in the slow pathway to allow the recovery of excitability of the fast pathway. Interestingly, in the second case, during an AVRT the atrial impulse suddenly proceeded alternately over the fast and the slow pathway. The progressive slowing of conduction over the slow pathway until a certain point which allows the recovery of excitability of the fast pathway determines the AVNRT. This is a case of "tachycardia-induced tachycardia" as confirmed by the fact that the ablation of the accessory pathway eliminated both tachycardias.     

"Left-variant" atypical atrioventricular nodal reentrant tachycardia: electrophysiological characteristics and effect of slow pathway ablation within coronary sinus

Introduction: Recent anatomical and electrophysiological studies have demonstrated the presence of leftward posterior nodal extension (LPNE); however, its role in the genesis of atrioventricular nodal reentrant tachycardia (AVNRT) is poorly understood. This study was performed to characterize successful slow pathway (SP) ablation site and to elucidate the role of LPNE in genesis of atypical AVNRT with eccentric activation patterns within the coronary sinus (CS).
Methods and Results: Among 45 patients with atypical AVNRT (slow-slow/fast-slow/both = 20/22/3 patients) with concentric (n = 37, 82%) or eccentric CS activation (n = 8, 18%), successful ablation site was evaluated. Among 35/37 patients (95%) with concentric CS activation, ablation at the conventional SP region outside CS eliminated both retrograde SP conduction and AVNRT inducibility. Among eight patients with eccentric CS activation, the earliest retrograde atrial activation was found at proximal CS 16 ± 4 mm distal to the ostium during AVNRT. The earliest retrograde activation site was located at inferior to inferoseptal mitral annulus, consistent with the presumed location of LPNE. Ablation at the conventional SP region with electroanatomical approach only rendered AVNRT nonsustained without elimination of retrograde SP conduction in seven of eight patients (88%). Ablation targeted to the earliest retrograde atrial activation site within proximal CS (15 ± 4 mm distal to the ostium); however, eliminated retrograde SP conduction and rendered AVNRT noninducible in six of eight patients (75%).
Conclusion: In 75% of "left-variant" atypical AVNRT, ablation within proximal CS was required to eliminate eccentric retrograde SP conduction and render AVNRT noninducible, suggesting LPNE formed retrograde limb of reentrant circuit.     

房室结双径路合并房室旁路的折返性心动过速及射频消融治疗

目的本研究旨在探讨房室结双径路（ＤＡＶＮＰ）合并房室旁路（ＡＰ）的电生理特征和射频消融要求。方法对２１８例阵发性室上性心动过速（ＰＳＶＴ）进行电生理检查，观察ＰＳＶＴ的前传和逆传途径，然后对ＡＰ或房室结慢径（ＳＰ）进行消融治疗。结果２１８例ＰＳＶＴ中检出ＤＡＶＮＰ＋ＡＰ１０例，检出率为４．６％。其中ＳＰ前传、ＡＰ逆传（ＳＰ－ＡＰ折返）４例，快径（ＦＰ）前传、ＡＰ逆传（ＦＰ－ＡＰ折返）１例，ＳＰ－ＡＰ折返并ＦＰ－ＡＰ折返或ＳＰ／ＦＰ交替前传折返４例，ＳＰ前传、ＦＰ逆传（ＡＰ旁观）１例。１０例患者均作ＡＰ消融，诱发房室结折返性心动过速（ＡＶＮＲＴ）的３例加作ＳＰ消融，术后随访均无复发。结论ＤＡＶＮＰ合并ＡＰ者ＡＰ均作为逆传途径，阻断ＡＰ是消融关键；ＡＰ旁观者也应作ＡＰ消融；仅有ＡＨ跳跃延长者不必接受房室结改良；ＡＰ消融者应作ＤＡＶＮＰ电生理检查。     

快慢型房室结折返性心动过速的电生理机制和经导管射频消融

目的探讨快慢型房室结折返性心动过速(AVNRT)的电生理机制和经导管射频消融。方法快慢型AVNRT消融患者42例。消融方法为在心室起搏或心动过速时标测最早逆传慢径心房激动部位,然后在窦性心律下或心动过速时消融。消融成功的标准为消除逆传慢径、1:1前传慢径及不能诱发任何类型AVNRT。结果所有42例均消融成功。逆传慢径消融成功部位在三尖瓣环和冠状静脉窦(CS)口之间(传统慢径区域)36例(86%),其最早逆传心房激动也位于上述区域;逆传慢径在CS近端或/和二尖瓣环心房侧消融成功6例(14%),其最早逆传心房激动多位于CS近端1～3cm处。结论多数快慢型AVNRT可在传统慢径区域(房室结右侧后延伸)消融成功,但部分病例需要在CS近端和/或二尖瓣环房侧(左侧后延伸)消融成功。     

快-慢型房室结折返性心动过速的电生理特征和射频消融治疗

报道８例快－慢型房室结折返性心动过速（ＡＶＮＲＴ）的电生理特征及射频消融治疗。其中３例为慢－快型ＡＶＮ－ＲＴ射频消融改良慢径后出现的快－慢型ＡＶＮＲＴ。８例均经消融慢径而成功终止心动过速。平均放电次数３±１．１次、平均放电时间１２０±３０．４ｓ、平均放电功率３０±１１Ｗ。随访６～２４个月，无复发。快－慢型ＡＶＮＲＴ具有以下临床电生理特征：①快径不应期短、慢径不应期长。②心内电刺激无房室结双径路现象。③心动过速能由心房刺激诱发。④心动过速时ＡＨ间期＜ＨＡ间期，冠状窦近端Ａ波最提前。熟悉快－慢型ＡＶＮＲＴ的电生理特征，对于鉴别房性心动过速及右后间隔旁道参与的房室折返性心动过速十分重要，也是指导快－慢型ＡＶＮＲＴ射频消融成功的关键。     

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.     

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.     

Radiofrequency Catheter Ablation of AtypicalAtrioventricular Nodal Reentrant Tachycardia

Ablation of Atypical Atrioventricular Nodal Reentrant Tachycardia, Introduction: Published reports of radiofrequency ablation of atypical atrioventricular nodal reentranttacbycardia (AVNRT) have been limited. We present our experience in 10 consecutive patientswith atypical AVNRT wbo underwent radiofrequency ablation of the "slow" AV nodal pathway.
Methods and Resttlts: there were 9 females and 1 male; their mean age was 44 ± 19 years (± SD), the mean AVNRT cycle length and ventriculoatrial (VA) interval at the His positionduring AVNRT were 340 ± 50 msec and 200 ± 70 msec, respectively. the slow pathway wassuccessfully ablated in all patients with a mean of 10 ± 7 radiofrequency energy applications inthe posteroseptal right atritim near the coronary sinus os. The mean procedure duration was 100 ± 35 minutes. There were no complications. In 4 patients, target sites were identified during sinus rhythm by mapping for possible slow pathway potentials, In the other 6 patients, target sites were identified by mapping retrograde atrial activation during AVNRT or ventricularpacing, The VA times at successful target sites were a mean of 45 ± 30 msec less tban the VAtime at the His cathetcr during AVNRT, There were no differences in success rate, number ofradiofrequency energy applications, or procedure duration between patients in whom mappingwas guided by possible slow pathway potentials or by retrograde atrial activation, During 6 ± 3 months of followup, 1 patient bad a recurrence of atypical AVNRT and underwent a secondablation procedure, which was successful.
Conclusion: Radiofrequency ablation of atypical AVNRT can be safely and effectivelyaccomplisbed when target sites are identified based either on possible slow pathway potentialsduring sinus rbytbm or retrograde atrial activation times during tachycardia.     

主动脉无冠窦内射频消融前间隔房室旁路

目的 报道经主动脉无冠窦内射频消融前间隔房室旁路.方法 7例患者,男性4例,女性3例,平均年龄（38.4±14.7）岁.电生理检查证实存在房室旁路,并检查其前传逆传功能和诱发旁路参与的房室折返性心动过速.在心动过速时标测最早心房逆传激动点作为消融靶点.结果 7例心动过速时最早心房激动部位均位于前间隔区域,但经右心房途径反复消融均不能成功阻断旁路,而在无冠窦内可标测到最早逆传心房激动点并消融成功,无并发症出现.结论 主动脉无冠窦内消融可作为治疗前间隔房室旁路的一种新途径,特别适用于右心房前间隔区域消融失败的病例.     

射频消融治疗房室结折返性心动过速的方法学研究——判断慢径阻断的新指标

改良房室结折返性心动过速 (AVNRT)慢径消融的方法学 ,以探讨判断慢径阻断的新指标。 6 0例AVNRT病人接受慢径射频消融术 ,根据X线影像部位和局部电图特点确定消融靶点 ,心房快速刺激 (S1S1)显示慢径前传放电消融 ,以 10s内慢径前传阻滞作为有效消融指标并以此连续放电达 30s。消融后房室结双径传导消失 ,不再诱发AVNRT为手术终点。 6 0例病人均达到消融终点。共消融 36 1个靶点 ,其中放电不足 10s者 2 80个、放电 30s者 81个 ,后者中 6 0个为有效消融靶点。有效阻断慢径者表现为放电 6 .9± 1.8(2 .8～ 10 )s慢径前传阻滞 ,S1刺激经快径前传。所有病人术后 3～ 7天食管电生理复查不再诱发AVNRT。随访 3～ 19个月无AVNRT复发。结论 :显示慢径前传消融可客观判断放电消融的有效性 ,避免盲目延长放电时间所造成的无效心肌损伤     

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.     

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.     

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.     

Anterograde slow pathway is not the same as retrograde slow pathway conducted in the reverse direction in patients with uncommon atrioventricular nodal reentrant tachycardia

INTRODUCTION: The aim of this study was to examine the location of anterograde and retrograde slow pathways in 16 patients with uncommon atrioventricular nodal reentrant tachycardia (AVNRT), including the fast-slow form in 10, slow-slow form in 5, and both fast-slow and slow-slow forms in 1. METHODS AND RESULTS: Patients were divided into two groups according to the approach used for slow pathway ablation in the initial radiofrequency catheter ablation (RFCA): one approach used earliest atrial activation during tachycardia (ES group, n = 9), and the other used a slow potential during sinus rhythm (SP group, n = 7). When the initial RFCA failed to eliminate slow pathway conduction in the ES group, an additional RFCA guided by a slow potential was performed. The ratio of lengths from the His-bundle region to the RFCA site and coronary sinus ostium (Abl/His-CS ratio) and the ratio of amplitudes of atrial and ventricular potentials at the RFCA site (A/V ratio) were compared between the two groups. In the initial RFCA, retrograde slow pathway conduction was eliminated without impairment of anterograde slow pathway conduction in 8 (89%) patients from the ES group, and bidirectional slow pathway conduction was eliminated in 6 (86%) patients from the SP group. Residual anterograde slow pathway conduction that was preserved after the initial RFCA in 8 of 9 patients was eliminated by an additional slow potential-guided RFCA. Both the Abl/His-CS ratio (0.86 +/- 0.07 vs 0.73 +/- 0.11, P = 0.01) and A/V ratio (0.80 +/- 0.31 vs. 0.14 +/- 0.01, P < 0.001) were higher in the ES group than the SP group. The ratios for the residual anterograde slow pathway ablation in the ES group were similar to those in the SP group. CONCLUSION: The results of this study suggest that the retrograde slow pathway runs more on the atrial side of the tricuspid valve annulus at the level of the coronary sinus ostium compared with the anterograde slow pathway, although both pathways run parallel or are fused in portions more proximal to the His bundle.