选择性慢径路消融前后心脏电生理变化

目的 比较房室结折返性心动过速患者行选择性射频消融（RFCA）慢径路术前、术后心脏各部分腔内电生理改变.方法 对房室结折返性心动过速患者在选择性慢径路RFCA前、后分别进行腔内电生理检查.记录RFCA前、后希氏束电图（HIS）、心房有效不应期（A-ERP）、心室有效不应期（V-ERP）、房室前传文氏阻滞点（AVN-WKB）、室房逆传文氏阻滞点（VAN-WKB）、房室结前传有效不应期（AVN-ERP）和房室结逆传有效不应期（VAV-ERP）,将RFCA前、后心脏各部分电生理参数进行分析比较.结果 RFCA前、后HIS电图A-ERP、V-ERP、AVN-ERP及VAN-WKB差异均无统计学意义（P＞0.05）,AVN-WKB、VAN-ERP差异有统计学意义（P＜0.05）.结论 选择性RFCA慢径路对房室结双径路疗效肯定.在RFCA前、后（急性期）房室前传、逆传电生理均有一定改变.这与RFCA改变了房室结的部分结构,如大部分病例慢径路消失有关,不同消融部位对房室结传导电生理改变产生不同结果.     

房室结慢径消融后对快径前传不应期影响

<正> 房室结双径路(DAVNP)是形成房室结折返性心动过速的必须电生理基础,射频消融房室结慢径路是治疗房室结折返性心动过速(AVNRT)安全、有效的方法.射频消融慢径路后有学者发现快径路前传不应期发生改变,本文对慢径路消融后快径路前传不应期改变,探讨慢径路消融后对快径路前传不应期的影响.1 资料和方法1.1 病例选择经电生理检查证实为DAVNP伴AVNRT患者44例,其中男性21例,女性23例;年龄15～77岁,平均年龄46.77±14.89岁;病史0.6～30年,均有反复发作室上性心动过速史.无器质性心脏病证据.合并房室结快径经消融者未选入.     

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。     

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。     

伴连续性房室结功能曲线的房室结折返性心动过速的电生理分析

目的：探讨无房室结双径路特性的房室结折返性心动过速(AVNRT)的电生理特点。方法：所有心动过速患射频消融前常规行心内电生理检查。结果：845例射频病人中325例为AVNRT，其中有21例患房室结功能曲线呈连续性，其电生理特征：希氏束图上心房回波(A)先出现，A波落在室波升支或其前，希氏柬不应期内刺激心室，不能提前夺获心房，射频消融后心房刺激时AHmax明显缩短。结论：伴连续性房室结功能曲线的AVNRT患心房刺激不表现房室结双径路的电生理特性，其消融终点初步定为：心房心室S1S1、S1S2刺激不诱发AVNRT；无AHvH传导曲线跳跃；房室结前传不应期明显缩短。     

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。     

伴连续房室结功能曲线的房室结折返性心动过速的电生理特点

目的：探讨不存在房室结双径路特性的房室结折返性心动过速（AVNRT）的电生理特点。方法：102例AVNRT患分为3组：A组15例,存在连续房室结功能曲线,心房递增起搏时无AH间期跳跃（≥5ms)延长;B组21例,存在连续房室结功能曲线,心房递增起搏时有AH间期跳跃（≥50ms）延长;C组64例,存在不连续房室结功能曲线。比较3组患射频消融前后心房递增起搏时最大AH间期[AHmax(WCL)]、心房期前刺激时最大AH间期[AHmax(ERP)]、房室结前向和逆向传导有效不应期（ERP）、保持房室1：1传导的心房／心室起搏周长和心动过速周长。结果：3组患消融后AHmax(WCL)和AHmax（ERP）均明显短于消融前（P＜0．01）。B组和C组的消融后房室结前向ERP明显增加,而组无明显变化。A组消融前AHmax和房室结逆向ERP、消融后AHmax下降程度以及心动过速周长均小于B组和C组患。结论：伴连续房室结功能曲线的AVNRT患,心房刺激可表现或不表现房室结双径路的电生理特性,射频消融后心房刺激时AHmax明显缩短提示已成功根治了AVNRT。     

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。     

房室结折返性心动过速诱发特点的观察

76例房室结折返性心动过速（AVNRT）患者中,55例采用一般程序刺激可诱发室上性心动过速（SVT）,消融后观察30min,心内电生理不能诱发;21例采用一般程序刺激不能诱发SVT,静滴异丙肾上腺素后能诱发SVT,消融后观察30min,静滴异丙肾上腺素后,再重复心内电生理仍无SVT发生.两组消融复发率无统计学意义;但一般刺激诱发组快慢径路之间有效不应期（ERP）有统计学差异;应用异丙肾上腺素后刺激诱发组基础快慢径ERP无统计学差异.程序刺激是否诱发AVNRT,与患者的房室结前传功能有关,即快慢径路前向传导的ERP相差越大,则越易发生AVNRT.消融中如一般刺激不能诱发,可静滴异丙肾上腺素后再行程序刺激诱发,这对判断消融成功终点及减少复发有较大意义.     

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     

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。     

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.     

Radiofrequency Ablation of a Concealed Nodoventricular Mahaim Fiber Guided by a Discrete Potential

INTRODUCTION: We present the case of a 17-year-old woman who underwent an electrophysiological study and radiofrequency (RF) ablation of supraventricular tachycardia refractory to medical treatment. Two right-sided, concealed, nondecremental atrioventricular accessory pathways (AV-APs) involved in orthodromic circus movement tachycardias were identified. After RF ablation of both AV-APs, evidence of bidirectional dual AV nodal conduction was demonstrated and regular narrow complex tachycardia was induced. METHODS AND RESULTS: During the tachycardia, retrograde slow and fast AV nodal pathway conduction with second-degree ventriculoatrial (VA) block and VA dissociation were observed. During the tachycardia with second-degree VA block, ventricular extrastimuli elicited during His-bundle refractoriness advanced the next His potential or terminated the tachycardia. Mapping the right atrial mid-septal region, a distinct high-frequency activation P potential was recorded in a discrete area, two thirds of the way from the His bundle toward the os of the coronary sinus. Detailed electrophysiologic testing with the recordable P potential demonstrated that the tachycardia utilized a concealed nodoventricular AP arising from the proximal slow AV nodal pathway. CONCLUSION: The tachycardia with slow 1:1 VA conduction could be reset by ventricular extrastimuli elicited during His-bundle refractoriness advancing the subsequent activation P potential and atrial activation. RF ablation guided by recording of the activation P potential resulted in elimination of both the slow AV nodal pathway and the nodoventricular connection with preservation of the normal AV conduction system.     

Localization of the Sites of Conduction Abnormalities in a Mouse Model of Myotonic Dystrophy

INTRODUCTION: A mouse strain lacking functional myotonic dystrophy protein kinase (DMPK) has recently been developed. DMPK-/- mice exhibit muscular and conduction abnormalities consistent with the disease; however, the site of abnormal cardiac conduction is unknown. METHODS AND RESULTS: Nine homozygous DMPK-/- mice and seven age matched wild-type (WT) controls underwent in vivo electrophysiologic studies using an endocardial 2-French catheter. Baseline intervals as well as Wenckebach and 2:1 cycle lengths were measured to assess AV and ventriculoatrial (VA) conduction. Effective refractory periods (ERP) and functional refractory periods were determined during atrial and ventricular premature stimulation. His-bundle recordings were obtained on all the studied animals (16/16). DMPK-/- mice had significantly prolonged PR (48.1 +/- 5.5 vs 40.9 +/- 3.9 msec, P = 0.010) and AH (36.7 +/- 4.0 vs 31.6 +/- 4.8 msec, P = 0.037) intervals compared to WT controls. HV intervals were very significantly prolonged as well (14.7 +/- 2.0 vs 10.3 +/- 0.8 msec; P < 0.0001). Three of 9 DMPK-/- and 1 of 7 WT mice exhibited VA block. Atrial ERP was reached before AV node ERP in 2 (22%) of 9 of the knockout mice and 5 (71%) of 7 of the controls (P = 0.06). Only one mouse (DMPK-/-) exhibited infra-Hisian block on premature atrial stimulation. CONCLUSION: In this mouse model of myotonic dystrophy, AV conduction abnormalities were localized to the supra-Hisian and infra-Hisian conduction tissues, with a higher predilection to the latter, a finding similar to the human form of the disease.     

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.     

Prolongation of the fast pathway effective refractory period during cryoablation in children: A marker of slow pathway modification

BACKGROUND: The fast pathway effective refractory period (ERP) has been reported to decrease after slow pathway modification with radiofrequency (RF) energy. How the fast pathway ERP changes during the ablation application has not been reported with either RF or cryoenergy. OBJECTIVES: Using the unique features of cryotherapy, this study assesses the short-term changes in fast pathway ERP during cryomodification of the slow pathway and examines whether these changes are a useful marker for successful slow pathway modification in children. METHODS: Nineteen pediatric patients (median age 15.1 years, range 9.6-19.6 years; weight 60.7 kg, range 35.6-130.2 kg) with anterograde dual AV nodal physiology underwent slow pathway modification with catheter-based cryoablation. Programmed stimulation was performed during cryoapplications after reaching -25 degrees C to assess fast pathway and slow pathway conduction. Data were analyzed from 59 of 237 cryoapplications where the fast pathway ERP was measured more than once (n = 13 patients). RESULTS: For 23 of 59 applications where the slow pathway was modified, the fast pathway ERP significantly increased during cryotherapy (Delta = 33.5 ms, P <.0001). The magnitude of fast pathway ERP prolongation during cryotherapy was larger when the slow pathway was modified than when there was no effect on slow pathway conduction (33.5 +/- 30.5 vs 5.8 +/- 18.9 ms, P =.0005). Prolongation of fast pathway ERP by >/=20 ms had 70% sensitivity and 72% specificity for predicting slow pathway modification. Following termination of cryoapplications, which resulted in slow pathway modification, the fast pathway ERP had significantly decreased from baseline (difference 44.5 ms, P <.0001). The effect on fast pathway ERP was not related to changes in cycle length during (R(2) = 0.04, P = .045) or after ablation (R(2) = 0.13, P = .012). CONCLUSION: The fast pathway ERP prolongs during cryoapplications that result in slow pathway modification and shortens after termination of cryoapplications. The magnitude of fast pathway ERP prolongation during cryoapplication may be useful as a marker for successful slow pathway modification.     

An anatomically guided approach to atrioventricular node slow pathway ablation.

Radiofrequency ablation of the "slow" pathway of the atrioventricular (AV) node reentrant circuit may be guided by electrophysiologic ("slow pathway potential") or anatomic landmarks. Experience with a systematic, anatomically guided approach in 25 patients (20 women and 5 men, aged 38 +/- 15 years) with typical AV node reentry is described. The slow pathway is assumed to be the posterior input to the AV node, approaching the nodal region in the corridor between the tricuspid annulus and the orifice of the coronary sinus. A series of radiofrequency lesions are given to interrupt this corridor at its entrance to Koch's triangle. If this is unsuccessful, the series of lesions are repeated progressively at higher levels approaching the AV node. The major end point for success is elimination of the slow pathway as determined by extrastimulus testing. A mean of 1.2 +/- 0.2 ablative sessions (20 +/- 12 applications of energy) achieved clinical success in 24 of 25 patients (96%) at a follow-up of 8.6 +/- 2.2 months. Anterograde Wenckebach cycle length increased from 361 +/- 67 ms to 398 +/- 70 ms (p = 0.01), yet the atrio-Hisian interval in sinus rhythm did not change (69 +/- 17 ms before vs 65 +/- 15 ms after ablation), p = 0.22. Retrograde Wenckebach cycle length was not affected (348 +/- 78 ms before vs 366 +/- 82 ms after ablation). During ablation, transient third-degree AV block occurred in 6 patients with no permanent sequelae. This approach provides a systematic, expedient technique to eliminate slow pathway conduction based on anatomic landmarks.     

Cure of Incessant Pacemaker Circus Movement Tachycardia by Radiofrequency Catheter Ablation

Ablation of Pacemaker Circus Movement Tachycardia. Introduction : Treatment of pacemaker circus movement tachycardia (PCMT) in patients with very long VA conduction times may present a problem.
Methods and Results : PCMT occurred in a 46-year-old woman with an uncommon AV nodal reentrant tachycardia who developed 2:1 AV block after fast pathway radiofrequency catheter (RF) ablation performed at another institution. Due to the long VA conduction time, PCMT could not be prevented by reprogramming the pacemaker or by the addition of antiarrhythmic drugs. Cure of the PCMT was obtained after selective RF ablation of the slow AV nodal pathway.
Conclusion : RF ablation of the retrograde conduction offers another alternative for treatment of PCMT.     

Intrinsic sinus and atrioventricular node electrophysiologic adaptations in endurance athletes

OBJECTIVES: In the present study, we evaluated sinus and atrioventricular (AV) node electrophysiology of endurance athletes and untrained individuals before and after autonomic pharmacologic blockade. BACKGROUND: Endurance athletes present a higher prevalence of sinus bradycardia and AV conduction abnormalities, as compared with untrained individuals. Previous data from our laboratory suggest that nonautonomic factors may be responsible for the longer AV node refractory period found in well-trained athletes. METHODS: Six aerobically trained male athletes and six healthy male individuals with similar ages and normal rest electrocardiograms were studied. Maximal oxygen uptake (O(2)max) was measured by cardiopulmonary testing. The sinus cycle length (SCL), AV conduction intervals, sinus node recovery time (SNRT), Wenckebach cycle (WC) and anterograde effective refractory period (ERP) of the AV node were evaluated by invasive electrophysiologic studies at baseline, after intravenous atropine (0.04 mg/kg) and after addition of intravenous propranolol (0.2 mg/kg). RESULTS: Athletes had a significantly higher O(2)max as compared with untrained individuals. The SCL was longer in athletes at baseline, after atropine and after the addition of propranolol for double-autonomic blockade. The mean maximal SNRT/SCL was longer in athletes after atropine and after propranolol. The WC and anterograde ERP of the AV node were longer in athletes at baseline, after atropine and after propranolol. CONCLUSIONS: Under double-pharmacologic blockade, we demonstrated that sinus automaticity and AV node conduction changes of endurance athletes are related to intrinsic physiology and not to autonomic influences.