房室结慢径消融术后快径前传不应期变化与房室结传导特性的关系

目的对房室结慢径消融术后快径路前传不应期的变化与房室结传导特性的关系进行分析。方法分别测量４５例房室结折返性心动过速患者术前快径路前传不应期（ＦＥＲＰＢ）、术后快径路前传不应期（ＦＥＲＰＡ）及其差值（ＤＥＲＰ）,术前慢径路前传时间（Ｓｐ）、快径路前传时间（Ｆｐ）及其差值（Ｄｐ）,并对ＦＥＲＰＢ与ＦＥＲＰＡ进行样本均数ｔ检验,计算ＤＥＲＰ与Ｄｐ的相关系数（ｒ）。结果ＦＥＲＰＢ与ＦＥＲＰＡ分别为３５４±５８．２５ｍｓ及３１１．１４±５７．３３ｍｓ（Ｐ＜０．０１）,ＤＥＲＰ与Ｄｐ呈正相关（ｒ＝０．３９８９,Ｐ＝０．０２～０．０５）。结论慢径消融术后快径路前传不应期缩短,快慢径路传导特性的差异与慢径路消融术后快径路前传不应期的变化有关。     

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…     

房室结改良术中快径消融的问题剖析

分析１３例慢－快型房室结折返性心动过速（ＡＶＮＲＴ）患者快径消融产生的问题：发生ＩＩＩ度房室传导阻滞（ＡＶＢ）２例（１５．４％）；术后出现促心律失常的不良后果２例（１５．４％），其中１例因仅阻断快径前传，逆传仍保留而使ＡＶＮＲＴ较术前更易发作，另１例快径前传、逆传部被阻断，因合并隐匿性旁道而使房室折返性心动过速更易发生。４例成功而留有Ｉ度ＡＶＢ者，因心电图不正常而给患者带来一定的心理负担。     

射频消融治疗以快慢径交替前传为电生理特征的房室结双径路（附2例报告）

房室结折返性心动过速 (ＡＶＮＲＴ)其发生机制国内外文献报道不少 ,早在 6 0- 70年代电生理及解剖资料证实了房室结系统的双径路 (α、β通道 )的存在 ,并阐明了ＡＶＲＮＴ发生机制主要是由传导速度快 ,不应期长的快径 (β通道 )和传导慢 ,不应期短的慢径 (α通道 )参与所决定 ,其特点是有“跳跃现象”和‘房性回波’[1] 。而以快慢径交替前传为电生理特征的房室结双径路却较少报道。本文2例患者在发生ＡＶＮＲＴ后电生理检查时反复再现快慢径交替前传并行射频消融治疗获得成功 ,说明了房室结双径路仍存在其他一些特点 ,具备这些特点的患者…     

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     

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。     

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。     

射频导管消融治疗房室结折返性心动过速中较难病例的电生理特点

目的：明确射频导管消融治疗房室结折返性心动过速（ＡＶＮＲＴ）中较难病例的电生理特点。方法：７２例行慢径射频导管消融的慢—快型ＡＶＮＲＴ病人中１１例（１５％）成功射频导管消融的放电次数超过２０次或总放电时间超过２００秒被定义为较难病例（较难组），其余的为非较难病例（非较难组）６１例（８５％）。结果：较难组１１例中有７例（６４％）短心房—希氏束间期（≤６０ｍｓ），而非较难组６１例中１４例（２３％）短心房—希氏束间期（≤６０ｍｓ，Ｐ＜０．０５）；较难组１１例中８例（７３％）短房室结逆传文氏周期（≤２８０ｍｓ）；非较难组５７例（６１例中有４例因心室刺激反复诱发心动过速不能测得逆传文氏周期）中有１５例（２６％）具有短房室结逆传文氏周期（≤２８０ｍｓ，Ｐ＜０．０１）。７２例中５５例（７６％）具有房室结前传不连续曲线。房室结前传曲线有多次“跳跃”在较难组１１例中有７例（６４％）病人，在非较难组中有１２例病人（２０％，Ｐ＜０．０１）。结论：短心房—希氏束间期、短房室结逆传文氏周期和前传曲线多次“跳跃”的病人在较难组所占的百分率明显高于非较难组，有显著差异。     

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。     

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     

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.     

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。     

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。     

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.     

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。     

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.     

"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.