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     

房室结折返性心动过速的可能折返机制和分型及其在指导慢径消融中的意义

目的根据房室结存在快径、右侧后延伸（经典慢径）和左侧后延伸（另一条慢径）和折返环路,对房室结折返性心动过速（AVNRT）进行分型,并根据电生理检查和射频消融的结果验证以上分型,同时分析此分型在指导房室结慢径消融中的意义.方法 812例入院进行射频消融AVNRT患者,常规行程序心房和心室电刺激和心内标测.根据AVNRT的类型分别采用消融房室结前传慢径和/或逆传慢径的方法治疗AVNRT.结果采用目前常用的AVNRT的分型方法,812例AVNRT患者中,慢快型659例（81%）、慢慢型81例（10%）、快慢型72例（9%）.所有812例AVNRT患者均消融或改良房室结慢径成功.按AVNRT可能的6种折返环路分型,慢快型649例（80%）、左侧变异慢快型10例（1%）、快慢型和变异快慢型57例（7%）、左侧变异快慢型15例（2%）、慢慢型81例（10%）.结论按房室结快径、右侧后延伸和左侧后延伸可能形成的6条折返环路,对AVNRT进行分型,符合电生理检查和射频消融的结果.此分型对理解AVNRT的折返机制和指导房室结慢径消融治疗AVNRT有较大的意义.     

典型与非典型房室结折返性心动过速折返环路的对比研究

背景：既往证据显示典型(慢-快型)与非典型(快-慢型)房室结折返性心动过速(AVNRT)并非经同一快径传导,然而对于同时合并典型与非典型AVNRT患者是否也是如此目前尚无证据。本研究通过对比同时合并典型与非典型AVNRT患者的传导间期,进一步探讨两种类型心动过速时慢、快径的特性,以阐明这一问题。方法：入选568例能够在电生理检查过程中通过程控起膊、自律性刺激或自然发生的AVNRT患者中,筛选出26例同时合并典型与非典型AVNRT的患者。通过直接测量慢-快型及快-慢型AVNRT心动过速时的传导间期,间接推算两种心动过速时快径传导时间,比较二者的差异,验证心动过速时经同一快径传导的假设。结果：患者平均年龄40.7±10.3(28-63)岁 ,其中女性14例(53.8%)。在典型ANVRT及非典型AVNRT时,心动过速周长(CL)分别为368.9±43.1、372.6±41.8 ms;心房最早逆传激动点位于冠状静脉窦口(CSO)比例分别为58%、67%;16例(61.5%)患者为快-慢型;慢-快型及快-慢型AVNRT心动过速时快径逆传与前传时间差别为21.68±10.34 ms,差异有统计学意义(P<0.05)。结论：典型和非典型AVNRT时并不完全通过同一快径逆传或前传。     

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。     

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。     

腺苷终止房室结和房室旁道折返性心动过速的心内电生理评价

探讨腺苷对阵发性室上性心动过速 (PSVT)的终止效果 ,观察PSVT终止后出现的心律失常。 2 5例患者 ,其中房室结折返性心动过速 (AVNRT) 11例、房室折返性心动过速 (AVRT) 14例 ,于心内电生理检查时 ,由前臂静脉注射(简称静注 )腺苷 6～ 12mg ,观察其终止心动过速的疗效和作用部位。结果 :11例AVNRT患者静注腺苷后 ,10例恢复窦性心律 ,其中 9例终止AVNRT于慢径前传 ,1例于快径逆传 ;14例AVRT患者静注腺苷后 ,14例均恢复窦性心律 ,终止AVRT 12例于房室结前传 ,2例于旁道逆传。心动过速终止后最常出现的心律失常是房性早搏和一过性Ⅰ和Ⅱ度房室阻滞 ;此外 ,室性早搏也很常见 ,部分患者可出现短阵室性心动过速 ,1例患者出现预激综合征伴心房颤动。结论 :腺苷终止PSVT有较高的成功率 ,但有潜在的促心律失常作用。     

慢快型房室结折返性心动过速的诱发及终止方式

慢快型房室结折返性心动过速（AVNRT）是阵发性室上性心动过速的另一常见类型，有时在体表心电图不易与顺向性房室折返性心动过速（AVRT）鉴别。了解慢快型AVNRT的诱发和终止方式及其电生理特征，在与AVRT的诊断及鉴别诊断方面有着重要的临床意义。     

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。     

逆向型房室折返性心动过速1例

宽QRS波群心动过速是心血管病常见的重症和急症,其中,逆向型房室折返性心动过速（AVRT）较少见。AVRT折返环路是以旁路为前传支、以正常房室传导系统为逆传,或由一支旁路下传,另一支旁路逆传;其心室激动的模式与真正的室性心动过速几乎无差别。通过回顾性分析逆向型房室折返性心动过速前后的心电图变化,明确AVRT的诊断需与室性心动过速区分开,临床应予以高度重视。心电图医师需熟悉心脏电生理的基本知识,与临床医师密切配合,在了解病史的基础上全面综合分析,才能及时地做出正确诊断。     

快径间断逆传是房室结折返性心动过速的少见电生理表现

报道 4例房室结折返性心动过速 (AVNRT)的少见电生理表现———快径间断逆传。 4例经心电图和食管电生理检查证实为AVNRT的病人 ,心内电生理检查中心室刺激无快径逆传 ,遂静脉注射异丙肾上腺素和消融阻断慢径后观察室房 (VA)传导特点。结果 :4例病人基础电生理检查均无快径逆传。静脉注射异丙肾上腺素后心室刺激 ,3例显示快径逆传并诱发AVNRT ,1例仍不显示快径逆传。消融阻断慢径后 ,4例病人均显示良好的快径逆传。结论 :快径间断逆传是AVNRT的少见电生理特点 ,慢径和快径相互干扰是其产生的重要机制之一。     

Unique electrophysiologic characteristics of atrioventricular nodal reentrant tachycardia with different ventriculoatrial block patterns: Effects of slow pathway ablation and insights into the location of the reentrant circuit

BACKGROUND: The electrophysiologic mechanisms of different ventriculoatrial (VA) block patterns during atrioventricular nodal reentrant tachycardia (AVNRT) are poorly understood. OBJECTIVES: The purpose of this study was to characterize AVNRTs with different VA block patterns and to assess the effects of slow pathway ablation. METHODS: Electrophysiologic data from six AVNRT patients with different VA block patterns were reviewed. RESULTS: All AVNRTs were induced after a sudden AH "jump-up" with the earliest retrograde atrial activation at the right superoparaseptum. Different VA block patterns comprised Wenckebach His-atrial (HA) block (n = 4), 2:1 HA block (n = 1), and variable HA conduction times during fixed AVNRT cycle length (CL) (n = 1). Wenckebach HA block during AVNRT was preceded by gradual HA interval prolongation with fixed His-His (HH) interval and unchanged atrial activation sequence. AVNRT with 2:1 HA block was induced after slow pathway ablation for slow-slow AVNRT with 1:1 HA conduction, and earliest atrial activation shifted from right inferoparaseptum to superoparaseptum without change in AVNRT CL. The presence of a lower common pathway was suggested by a longer HA interval during ventricular pacing at AVNRT CL than during AVNRT (n = 5) or Wenckebach HA block during ventricular pacing at AVNRT CL (n = 1). In four patients, HA interval during ventricular pacing at AVNRT CL was unusually long (188 +/- 30 ms). Ablations at the right inferoparaseptum rendered AVNRT noninducible in 5 (83%) of 6 patients. CONCLUSION: Most AVNRTs with different VA block patterns were amenable to classic slow pathway ablation. The reentrant circuit could be contained within a functionally protected region around the AV node and posterior nodal extensions, and different VA block patterns resulted from variable conduction at tissues extrinsic to the reentrant circuit.     

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.     

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。     

Characterization of subforms of AV nodal reentrant tachycardia.

BACKGROUND: Different subforms of AV nodal reentrant tachycardia (AVNRT) have been described ("Slow/Fast", "Slow/Slow" and "Fast/Slow"). Our aim is to improve definition of these subforms, based on systematic evaluation, in a large cohort of patients, of the site of earliest atrial activation, timing intervals, and evidence for the presence or absence of a lower common pathway (LCP). METHODS AND RESULTS: In 344 patients, AVNRT using a slow pathway (SP) for antegrade conduction and earliest atrial activation at the superior septum (i.e. retrograde fast pathway) was present in 81.4% (Slow/Fast). AVNRT using an SP for antegrade conduction and earliest atrial activation at the inferior septum or proximal coronary sinus (i.e. retrograde slow pathway; Slow/Slow) was present in 13.7%. AVNRT with a short A-H interval and retrograde SP conduction (Fast/Slow) was present in 4.9%. All timing intervals during tachycardia are dependent on autonomic tone. H-A intervals during tachycardia (H-A(t)) overlap in Slow/Slow and Slow/Fast AVNRT: Slow/Slow therefore may mimic Slow/Fast AVNRT. The H-A interval during pacing at the tachycardia cycle length (H-A(p)) better discriminates both subforms. The difference between H-A(p) and H-A(t) (Delta H-A) was significantly longer in Slow/Slow compared with Slow/Fast AVNRT (isoprenaline 0.5 microg/min: 27+/-18 ms vs. 1+/-9 ms; p<0.001). Delta H-A>15 ms had a specificity and sensitivity for Slow/Slow of 94% and 64%, respectively. A Delta H-A>15 ms, combined with other data, pointed to the presence of a long LCP in 36 of 43 evaluable Slow/Slow (84%) and all Fast/Slow, but in only 10% of Slow/Fast (p<0.001). Retrograde conduction during ventricular pacing at the tachycardia cycle length was present in only 6% of Fast/Slow. CONCLUSIONS: AVNRT subforms can be distinguished based on a systematic evaluation of atrial activation sequence, timing intervals and evidence for the presence of an LCP.     

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.     

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.     

Atrial tachycardia with slow pathway conduction mimicking typical atrioventricular nodal reentrant tachycardia.

A 68-year-old woman with palpitations underwent electrophysiologic testing. During burst atrial pacing the PR interval exceeded the RR interval and induced a supraventricular tachycardia consistent with a typical AV nodal reentrant tachycardia (AVNRT). Radiofrequency ablation of the slow pathway during the tachycardia immediately produced 2 : 1 AV conduction. After slow AV nodal pathway ablation an atrial tachycardia (AT) remained inducible with the earliest atrial activation around the HB region. Radiofrequency ablation at the site of earliest atrial activation interrupted the AT without AV block. AT originating from the HB region with slow pathway conduction may mimic typical AVNRT.     

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。