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。     

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.     

关于房室结折返性心动过速慢径消融终点的探讨

534例慢-快型房室结折返性心动过速(AVNRT)患者行慢径消融治疗,观察A型终点(彻底消融慢径)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。A、B型分别复发5例(1.2%)、11例(9.4%),差异有统计学意义。B型终点的未复发与复发患者相比,其房室结前传文氏周期、快径前传有效不应期和房室结双径路的跳跃增值缩短。认为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。     

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。     

射频消融房室结前传慢径治疗慢-慢型房室结折返性心动过速

慢 慢型房室结折返性心动过速 (ＡＶＮＲＴ)用前传慢径和逆传慢径构成心动过速折返环。目前较常用消融逆传慢径心房插入点 ,但复发率高达 1 0 %左右。笔者推测 ,由于慢 慢型ＡＶＮＲＴ前传慢径的传导时间长 ,有效不应期短 ,可能为维持慢 慢型ＡＶＮＲＴ折返环的关键支 ,用解剖法消融前传慢径 ,可能与常见慢 快型ＡＶＮＲＴ消融前传慢径的方法一样有效。1 .资料与方法 :2 0 0 0年 1月～ 2 0 0 1年 1 1月 ,因ＡＶＮＲＴ入院行经导管射频消融术患者 1 4 5例 ,其中慢 慢型 1 0例(6 9% )。放置 1 0极冠状静脉窦 (ＣＳ)导管至ＣＳ ,4极导管分别…     

慢慢型房室结折返性心动过速的电生理机制和射频导管消融治疗

目的　探讨慢慢型房室结折返性心动过速 (AVNRT)的电生理机制和不同射频导管消融方法的治疗效果。方法　812例AVNRT患者分为两组,第 1组 500例,比较慢慢型中前传慢径和逆传慢径的成功消融部位的异同、比较在慢慢型和快慢型中选择性地消融逆传慢径部位的异同。第 2组312例,在设想慢慢型AVNRT折返机制的基础上,前瞻性地对慢慢型仅选择性消融前传慢径而不消融逆传慢径。结果　第 1组 59例慢慢型AVNRT的前传和逆传慢径的传导时间和成功消融的部位明显不同,逆传慢径多在冠状静脉窦(CS)窦口内或CS近端消融成功,而前传慢径多在三尖瓣环和CS窦口之间消融成功;慢慢型与快慢型的逆传慢径有明显不同的传导时间、递减特性和解剖分布。在第 2组前瞻性地仅消融前传慢径治疗 22例慢慢型组中,在三尖瓣环和CS窦口之间成功消融前传慢径并治愈AVN RT后, 21例逆传慢径功能不变,其逆传慢径最早心房插入点部位与前传慢径消融部位不同。所有 812例AVNRT均消融成功,第 1组在 3年以上的随访中, 387例慢快型复发 1例 (0 3% ), 59例慢慢型复发6例(10% ), 54例快慢型无复发。第 2组 312例 3 ~48 ( 23±12 )个月的随访中,慢快型复发 2例(0 5% ),慢慢型和快慢型无复发。结论　(1)慢慢型AVNRT应用电生理特性和解剖分布不同的两条慢径形     

射频消融慢径对房室结前传文氏周期的影响

目的：分析射频消融房室结慢径后对房室结前传文氏周期的影响。方法：67倒房室结折返性心动过逮患者，进行了选择性房室结慢径消融，除1例失破外，66例消融成功，其中45例清融后慢径不存在(Ⅰ组)，12例消融后残存慢径前恃功能(Ⅱ组)。结果：消融后快径有效不应期在Ⅰ组显著变短(331±74ms vs 271±77ms，P<0．001)，在Ⅱ组无显著变化(346±49ms vs 314±50ms，p=NS)。房室结前传文氏周期消融前、后无显著变化(Ⅰ组352±60ms vs 337±71ms，P—NS,Ⅱ组350±48ms vs 343±67ms，P—NS)。在Ⅰ组，消融前、后快径前传有效不应期与房室结前传文氏周期呈正相关(清融前r=0．692，P<0．001；消融后r=0．854，P<0．001)。在Ⅱ组，消融后慢径前传有效不应期与房室结前传文氏周期无相关性(r=0．497，p<0．10)，快径前传有效不应期与房室结前传文氏周期呈正相关(r=0．838，p<0．02)。结论：射频消融慢径对房室结前传文氏周期影响不大，但明显使怏径有效不应期缩短。     

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。     

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。     

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.     

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.     

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。     

Effects of atropine on induction and maintenance of atrioventricular nodal reentrant tachycardia.

The electrophysiologic effects of atropine were studied in 14 patients with dual atrioventricular (AV) nodal pathways and recurrent paroxysmal supraventricular tachycardia (PSVT). During PSVT, all patients used a slow pathway (SP) for antegrade and fast pathway (FP) for retrograde conduction. Atropine enhanced both SP antegrade and FP retrograde conduction, shown by a decrease in paced cycle lengths (atrial and ventricular) producing AV and ventriculoatrial block. Five patients had induction of sustained PSVT before and after atropine. Seven patients failed to induce or sustain PSVT before atropine, because of retrograde FP refractoriness. All seven had induction of sustained PSVT after atropine due to facilitation of FP retrograde conduction. Two patients had only single atrial echoes before atropine, reflecting SP antegrade refractoriness. After atropine, sustained PSVT was inducible in one, and nonsustained in the other, PSVT cycle length could be compared in seven patients before and after atropine and decreased from 383 +/- 25 to 336 +/- 17 (p less than 0.05). Thus, in patients with dual AV nodal pathways, atropine facilitated SP antegrade and FP retrograde conduction, shortened cycle length of PSVT and potentiated ability to sustain PSVT.     

Conduction properties of the antegrade fast and slow AV nodal pathways associated with AV nodal reentrant tachycardia.

To elucidate differences in conduction properties among the normal atrioventricular (AV) node and the antegrade fast and slow dual AV nodal pathways (DAVNPW), AV nodal conduction curves were analyzed quantitatively in 38 patients. Eighteen patients had antegrade DAVNPW with AV nodal reentrant tachycardia (AVNRT) (dual pathways group) and the remaining 20 had smooth AV nodal conduction curves, without evidence of AV nodal dysfunction (control group). The effective refractory period (ERP) of the antegrade fast pathway was longer than that of the normal AV node (at both basic cycle lengths of 700 and 500 msec, p less than 0.01). Although the atrial premature beats were delayed by a longer ERP in the fast pathway, there was no significant difference in the degree of prolongation of AV nodal conduction time related to shortening of the coupling interval (i.e., ratio of A2H2 increment to A1A2 decrement) between these two pathways. On the other hand, the ERP of the antegrade slow pathway was similar to that of the normal AV node. The degree of prolongation of AV nodal conduction time (relative to the shortening of the coupling interval) was greater in the antegrade slow pathway than in the normal AV node. In conclusion, these findings suggest that in DAVNPW with AVNRT: (1) the antegrade fast pathway is similar to the AV node and its conduction properties are unlikely to be better than those of the normal AV node and (2) the antegrade slow pathway has quantitatively poorer conduction properties than the normal AV node, since it has a greater degree of decremental conduction.     

Mechanism of induction of atrioventricular node reentry by simultaneous anterograde conduction over the fast and slow pathways

INTRODUCTION: AV node reentry (AVNRT) is typically induced with anterograde (Ant) block over the fast pathway (FP) and conduction over the slow pathway (SP), with subsequent retrograde (Ret) conduction over the FP. Rarely, a premature atrial complex (PAC) conducts simultaneously over the FP and SP to induce AVNRT (2 for 1). This study investigates the mechanism of 2 for 1 induction. METHODS AND RESULTS: Of 192 consecutive patients (pts) undergoing posteroseptal radiofrequency ablation to treat AVNRT, 4 pts (2%) had 2 for 1 AVNRT induction. All needed isoproterenol for AVNRT initiation, and Ant conduction was over the SP during AVNRT. Controls (n = 15) were randomly selected from the remaining 188 pts and required isoproterenol to induce AVNRT with Ant block over the FP. For 2 for 1 versus control, respectively, there was no difference in mean age (55 vs. 46 yr), AVNRT cycle length (420 vs. 320 ms), or the Ant effective refractory period of the FP (320 vs. 344 ms). Of note, the PAC that induced AVNRT had a significantly longer AH interval over the SP in pts with 2 for 1 versus control (470 vs. 320 ms, P = 0.016), even though the A1A2 interval for induction was longer for 2 for 1 (315 vs. 260 ms, P = 0.003). Ret conduction over the SP was relatively poor in the 2 for 1 group as evidenced by 4/4 pts with induction of AVNRT during incremental ventricular pacing versus only 1/15 control pts (P < 0.001). CONCLUSION: The unique induction of AVNRT by a PAC with simultaneous conduction over the FP and SP is best explained by minimal to no retrograde invasion of the SP from the anterogradely conducted fast pathway impulse, and consistent with this observation is the initiation of slow/fast AVN reentry during incremental RV pacing.     

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.     

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.