选择性消融逆传快径治疗典型房室结折返性心动过速

设计一种新的射频消融方法（选择性消融逆传快径）对25例反复发作的典型房室结折返性心动过速（AVN－RT）进行消融治疗。经股静脉插入1～2很大头电极至Koch氏三角区,于旁His束心室起搏下寻找还传A’最早的靶点,靶点图上不能有或仅有极小H波,大头电极用力压向靶点出现：①VA分离或H’A’间期延长,说明逆传快径已被机械刺激所阻断,立即放电15～25W,持续30～90S;②AH间期延长,说明前传快径已被机械刺激所阻断,移开大头电极待AH间期恢复正常,再重新标测;③反复数次操作,大头电极的机械刺激仍不能阻断逆传快径,则选择逆传A’最早的靶点试放电30S,出现VA分离或H’A’间期延长,则放电至60～90s,否则重新标测靶点。消融终点为VA分离或H’A’间或延长,用异丙肾上腺素仍不能诱发典型和非典型AVNRT。25例均一次消融成功,逆传快径被阻断、前传慢径均保留;23例VA分离、2例仅有H’A’间期延长;6例前传快径阻断;4例病人术中大头电极的机械刺激阻断了逆传快径。1倒成功靶点位于His束电极后上方,24例位于His束电极与冠状窦电极之间的区域。结论：在仔细精确的电生理标测下可实现选择性消融逆传快径,保留前传快慢径。此方法安全有效。     

依赖异丙肾上腺素逆传的房室结折返性心动过速

目的探讨房室结双径路中的室房逆传和对房室结双径路的快径逆传间歇性的认识。方法对401例AVNRT者中,在基础状态下RVAS1S1>500ms为无室房逆传的13例患者进行异丙肾试验,重复电生理检查。结果401例AVNRT为慢快型,其中388例(96.8%)RVAS1S1<300ms,为有室房逆传组,而13例(3.2%)RVAS1S1>500ms,为无室房逆传组。结论AVNRT的病人中行电生理检查示房室结存在双径路而室房分离或室房传导时间长,在不能诱发心动过速时,应使用异丙肾上腺素以明确存在快径间歇性逆传的可能性。     

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.     

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。     

依赖异丙肾上腺素逆传的房室折返性心动过速

目的：探讨4例依赖异丙肾上腺素逆传的房室折返性心动过速的发作情况及电生理特点。方法：对4例射频导管消融前常规电生理检查未能诱发出阵发性定性心动过速及A－H间期跳跃，亦未见旁道逆传者，静脉滴注异丙肾上腺素、右心室刺激时发现左侧旁道逆传，并均诱发出正向型房室折返性心运过速；停止注射后，左侧旁道逆传功能消失，亦不能诱发出房室折返性心动过速。结果：静脉滴注异丙肾上腺素，右心室起搏下用逆行法于二尖瓣环心室侧消融，4例均获成功；术后静脉滴注异丙肾上腺素下再行右心室起搏，未见旁道逆传现象。结论：部分隐匿性旁道构成的房室折返性心动过速发作依赖异丙肾上腺素，射频导管消融在静脉滴注异丙肾上腺素及右心室起搏下进行。     

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.     

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?     

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。     

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。     

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     

Selective transcatheter ablation of the fast and slow pathways using radiofrequency energy in patients with atrioventricular nodal reentrant tachycardia.

BACKGROUND. The safety and efficacy of selective fast versus slow pathway ablation using radiofrequency energy and a transcatheter technique in patients with atrioventricular nodal reentrant tachycardia (AVNRT) were evaluated. METHODS AND RESULTS. Forty-nine consecutive patients with symptomatic AVNRT were included. There were 37 women and 12 men (mean age, 43 +/- 20 years). The first 16 patients underwent a fast pathway ablation with radiofrequency current applied in the anterior/superior aspect of the tricuspid annulus. The remaining 33 patients initially had their slow pathway targeted at the posterior/inferior aspect of the right interatrial septum. The fast pathway was successfully ablated in the initial 16 patients and in three additional patients after an unsuccessful slow pathway ablation. A mean of 10 +/- 8 radiofrequency pulses were delivered; the last (successful) pulse was at a power of 24 +/- 7 W for a duration of 22 +/- 15 seconds. Four of these 19 patients developed complete atrioventricular (AV) block. In the remaining 15 patients, the post-ablation atrio-His intervals prolonged from 89 +/- 30 to 138 +/- 43 msec (p less than 0.001), whereas the shortest 1:1 AV conduction and effective refractory period of the AV node remained unchanged. Ten patients lost their ventriculoatrial (VA) conduction, and the other five had a significant prolongation of the shortest cycle length of 1:1 VA conduction (280 +/- 35 versus 468 +/- 30 msec, p less than 0.0001). Slow pathway ablation was attempted initially in 33 patients and in another two who developed uncommon AVNRT after successful fast pathway ablation. Of these 35 patients, 32 had no AVNRT inducible after 6 +/- 4 radiofrequency pulses with the last (successful) pulse given at a power of 36 +/- 12 W for a duration of 35 +/- 15 seconds. After successful slow pathway ablation, the shortest cycle length of 1:1 AV conduction prolonged from 295 +/- 44 to 332 +/- 66 msec (p less than 0.0005), the AV nodal effective refractory period increased from 232 +/- 36 to 281 +/- 61 msec (p less than 0.0001), and the atrio-His interval as well as the shortest cycle length of 1:1 VA conduction remained unchanged. No patients developed AV block. Among the last 33 patients who underwent a slow pathway ablation as the initial attempt and a fast pathway ablation only when the former failed, 32 (97%) had successful AVNRT abolition with intact AV conduction. During a mean follow-up of 6.5 +/- 3.0 months, none of the 49 patients had recurrent tachycardia. Forty patients had repeat electrophysiological studies 4-8 weeks after their successful ablation, and AVNRT could not be induced in 39 patients. CONCLUSIONS. These data suggest that both fast and slow pathways can be selectively ablated for control of AVNRT. Slow pathway ablation, however, by obviating the risk of AV block, appears to be safer and should be considered as the first approach.     

异丙肾上腺素对射频消融房室结折返性心动过速疗效评价的意义

对消融房室结慢径的７２例房室结折返性心动过速（ＡＶＮＲＴ）病人进行观察分析，以了解异丙肾上腺素在ＡＶＮＲＴ射频消融中的临床价值。消融前电生理检查时有２７．８％（２０／７２）的病人未能诱发ＡＶＮＲＴ，静脉滴注异丙肾上腺素后，８５．０％（１７／２０）则能诱发；消融后４７．９％（３４／７２）用异丙肾上腺素评价，其中８例既有房室结跳跃现象又有心房回波的病人５０．０％（４／８）诱发出ＡＶＮＲＴ而重新消融。随访８．５±４．３个月，成功消融的７１例中，３４例经异丙肾上腺素评价者无一例复发，３７例未用异丙肾上腺素评价者２例复发。提示静脉滴注异丙肾上腺素可提高ＡＶＮＲＴ的诱发率；消融后房室结慢径前传功能存在时，无论有无心房回波均应用异丙肾上腺素评价，以确定消融终点和降低复发率。     

心动过速RR间期交替的发生机制及导管射频消融治疗

目的　分析QRS心动过速伴RR间期长短交替的发生机制及导管射频消融情况。方法　对 6例心动过速伴RR间期长短交替患者 ,常规行动态心电图及食管电生理检查。心内电生理检查提示存在房室旁路或房性心动过速伴房室结双径路 ,先进行旁路或房性心动过速的消融 ,消融成功后再进行心内电生理检查 (包括应用异丙肾上腺素进行心动过速诱发 ) ,如不能诱发心动过速则终止手术。若提示存在房室结多径路 ,则进行慢路径改良术。结果　食管电生理检查提示 :4例患者存在房室旁路伴房室结双径路 ;2例患者存在房室结三径路。心内电生理检查及消融结果显示 :3例患者为房室旁路伴房室折返性心动过速 ,成功消融后不能诱发房室结折返性心动过速 ;1例患者同时存在房室及房室结折返性心动过速 ,成功消融房室旁路后再改良慢路径 ;2例患者为房室结三径路 ,经慢径路改良后房室结传导曲线连续 ,未诱发心动过速。 6例患者无并发症发生 ,随访期间无心动过速发作。结论　室上性心动过速伴RR间期交替发生率较低 ,且均与房室结传导不连续有关。心动过速伴RR间期交替发生机制较为复杂 ,除了与房室结纵向传导的不连续有关外 ,还与其不应期密切相关。食管电生理检查与心内电生理检查相比对揭示RR间期交替的发生机制具有较高的诊断价值。     

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。     

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.     

心房起搏时PR与RR间期比值对阵发性室上性心动过速鉴别诊断的意义

为探讨快速心房起搏最短１∶１房室传导时最大ＰＲ间期（ＰＲｍａｘ）与ＲＲ间期比值（ＰＲｍａｘ／ＲＲ）在鉴别阵发性室上性心动过速中的意义，分析比较了２０例房室结折返性心动过速（ＡＶＮＲＴ，有房室结前传跳跃现象者１２例、无跳跃现象者８例）和２０例房室折返性心动过速（ＡＶＲＴ）患者消融前、后快速心房起搏时最短１∶１房室传导的ＰＲｍａｘ／ＲＲ。ＡＶＮＲＴ组消融前、后心房快速起搏时最短１∶１房室传导的ＰＲｍａｘ／ＲＲ为１．１２±０．１２和０．４２±０．０７，两者比较差异有高度显著性，Ｐ＜０．０１；ＡＶＲＴ组为０．５２±０．１６和０．５１±０．１８，两者比较差异无显著性，Ｐ＞０．０５。消融前，ＡＶＮＲＴ组ＰＲｍａｘ／ＲＲ与ＡＶＲＴ组相比有显著性差异（１．１２±０．１２ｖｓ０．５２±０．１６，Ｐ＜０．０１）。ＰＲｍａｘ／ＲＲ＞１诊断ＡＶＮＲＴ的敏感性为９０％、特异性９１％。提示ＰＲｍａｘ／ＲＲ＞１在消融前可用来鉴别ＡＶＮＲＴ与ＡＶＲＴ；对无房室结前传跳跃的ＡＶＮＲＴ，消融后ＰＲｍａｘ／ＲＲ＜１可作为慢径消融成功的指标     

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.