多种类型房室结折返性心动过速的机制和经导管射频消融治疗

目的分析多种类型房室结折返性心动过速并存患者的电生理机制和经导管射频消融治疗的结果。方法研究人群为18例经电生理检查后行射频消融治疗的多种类型房室结折返性心动过速(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逆传慢径的心房激动部位。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。结果多种类型AVNRT的发生率为1.8%(18/1000)。18例患者中有11例在消融治疗前的电生理检查中诱发出2种类型AVNRT,有7例在电生理检查中诱发出1种类型AVNRT,消融此型后又诱发出另外1种类型AVNRT。在消融前即诱发出2种类型AVNRT的10例患者,均在三尖瓣环与冠状窦口之间(房室结右侧后延伸)成功消融两种类型AVNRT。在电生理检查中出现1种类型AVNRT,经导管射频消融这种AVNRT后,又出现另外1种类型AVNRT的7例患者中,4例在三尖瓣环与冠状窦口之间(右侧后延伸)成功消融两种类型AVNRT;另3例中的2例在房室结右侧后延伸处消融后,第1种AVNRT不能诱发,但可诱发出另外1种类型AVNRT,经在冠状窦近端及二尖瓣环房侧(房室结左侧后延伸)进一步消融成功;另1例经消融三尖瓣环与冠状窦口之间(右侧后延伸)后,除原诱发的快慢型AVNRT外,还可诱发慢慢型AVN-RT,其逆传心房激动顺序与快慢型时相同,提示2种类型AVNRT均应用同一条逆传慢径,经在冠状静脉窦内和二尖瓣环房侧(房室结左侧后延伸)成功消融2种类型AVN-RT。术后随访18例均无复发。结论对于大多数多种类型AVNRT患者,具有前向和逆向传导功能的传统房室结慢径(房室结右侧后延伸)可能为多型AVNRT的主要基质,因此消融房室结右侧后延伸可成功消融大多数多型AVNRT。对于少部分多型AVNRT患者,左侧后延伸与右侧后延伸可能分别作?     

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.     

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。     

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     

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。     

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。     

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.     

怀疑AVNRT患者的经验性导管消融

目的探讨经验性慢径导管消融治疗临床疑似房室结折返性心动过速(AVNRT)的可行性。方法回顾分析本院1998年10月~2015年10月368例接受房室结慢径消融治疗患者的临床资料、电生理检查与导管射频消融治疗结果及随访结果,比较323例电生理检查证实存在房室结双径传导且能诱发AVNRT和45例存在房室结双径传导但不能诱发AVNRT患者的消融结果及平均7.8年随访期内心动过速复发率,另对21例疑似AVNRT但电生理检查无房室结双径传导,无可诱发心动过速,且未接受慢径消融治疗的患者进行了平均1.4年随访。结果经导管射频消融术中不能诱发AVNRT患者与术中能诱发心动过速患者首次慢径消融的成功率均为100%,且均无严重并发症发生;术中不能诱发心动过速患者随访期心动过速复发率(4.4%)高于术中能诱发AVNRT患者(1.5%)(p0.05%)。术中能诱发AVNRT患者消融后复发病例均为首次消融时未达到主要消融终点(A-H间期跳跃现象消失)者,术中未诱发心动过速患者消融后复发病例再次电生理检查时均未发现存在房室结双径传导现象,亦未再诱发心动过速。在平均1.4年随访期内38%的疑似AVNRT但未接受经验性慢径消融治疗的患者再次发生心动过速。结论对于电生理检查证实存在房室结双径传导但不能诱发心动过速的疑似AVNRT患者,经验性慢径导管消融治疗安全有效,但应尽量以A-H间期跳跃现象消失作为消融终点。对于电生理检查未证实存在房室结双径传导,且不能诱发心动过速的疑似AVNRT患者,应酌情选择经验性慢径导管消融治疗。     

快慢型房室结折返性心动过速的电生理特点

目的分析快慢型房室结折返性心动过速（AVNRT）患者的临床特征、心电网和电生理检查特点、射频消融治疗特点,旨在为临床长RP。心动过速鉴别提供帮助。方法11例经心内电生理检查证实为慢快型房室结折返性心动过速的患者,回顾性分析其临床特征、心电图特点及电生理检查特点及射频消融治疗。结果心动过速表现为窄QRs波心动过速,RP’〉P’R,P。在Ⅱ、Ⅲ、aVF导联倒置,RP’间期为350±25ms,心率为1664-30bpm。11例患者中有3例出现室房逆传跳跃现象。心房程序刺激无明显跳跃现象,11例均可由心房StS：刺激诱发心动过速发作,且容易诱发,容易终止。心动过速发作时,5例CS9．10A波最早,6例HiS的A波最早,其中1例静推ATP心动过速终止。11例患者中9例经房室结改良消融传统慢径获得成功,2例在冠状静脉窦内消融成功,术后随访3个月以上均未再发作心动过速。结论长RP’心动过速的诊断和鉴别诊断有一定困难,如能排除慢旁道和房速,应考虑快慢型房室结折返性心动过速。     

多种类型房室结折返性心动过速的电生理特点

目的 探讨多种类型房室结折返性心动过速（AVNRT）的电生理特征及消融体会。方法 回顾性分析成功行射频导管消融的113例AVNRT病人的临床和心内电生理资料。结果 113例AVNRT患者中6例存在多种类型AVNRT,其中存在2种、3种和4种类型AVNRT者各占2例,共有8种类型AVNRT;2例存在MAVNP,其余4例DAVNP阳性;均在慢径路区域行射频消融,放电时出现交界性早搏和/或心律,放电次数,功率、时间和X线曝光时间与同期慢-快型AVNRT相似,术后应用阿托品或异丙基肾上腺素未再诱发室上性心动过速,亦无回波,术中和术后均无房室传导阻滞,随访2.0-25.5月,无1例复发。结论 多种类型AVNRT并不少见,中径路既有逆传功能,也具有前传功能,多种类型AVNRT的射频消融类似于慢-快型AVNRT,安全有效。     

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.     

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.     

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.     

"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.     

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。     

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.