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射频消融房室结慢径治疗房室结折返性心动过速消融终点的探讨 总被引:4,自引:0,他引:4
消融房室结慢径是治疗房室结折返性心动过速(AVNRT)安全而有效的方法.但AVNRT消融终点标准意见不尽一致.本文分析163例AVNRT的射频导管消融术(RFCA)电生理特征及慢径消融时的心电改变,并对其消融的终点标准、消融方法学及并发症预防进行探讨. 相似文献
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目的初步探讨射频改良房室结双径路的能量,房室传导阻滞发生率,初步手术成功率和复发率.方法自1998年1月至2000年6月,对20例(女14例,男6例),平均年龄(43.4±17.1)岁频发房室结折返性心动过速(AVNRT)患者,采用射频消融能量从5W低能量开始,无效则按每5W逐渐递增,限定最大能量为30W进行消融慢径改良房室结功能.结果20例患者全部改良成功,平均释放能量5~30W,平均(17.6±7.2)W,术后平均4~30个月随访,无1例发生房室传导阻滞并发症,其中1例术后2个月复发AVNRT,经再次射频消融慢径改良房室结功能成功.结论采用低能量射频消融改良房室结功能,疗效满意,对减少房室传导阻滞并发症有益. 相似文献
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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。 相似文献
4.
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… 相似文献
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<正> 射频消融(Radiofrequency current ablation,RFCA)治疗房室结折返性心动过速(AVNRT)临床上已得到广泛开展,选择性消融慢径被一致认为是最安全、有效的方法.但有部分患者并发完全性房室传导阻滞,即使在有经验的心脏中心,其发生率仍为0~3%,可发生在消融过程中,亦可发生在消融术后.我们对我院开展RFCA工作以来发生的2例完全性房室传导阻滞病例进行了回顾分析,以避免今后发生完全性房室传导阻滞等并发症.1 资料和方法病例:对56例AVNRT病人进行了房室结慢径消融,其中2例出现Ⅲ°房室传导阻滞,均为男性,年龄分别为63岁、32岁,阵发性室上性心动过速病史超过十年,既往无器质性心脏病和传导阻滞病史. 相似文献
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房室结折返性心动过速射频消融有关问题的探讨 总被引:6,自引:0,他引:6
房室结折返性心动过速 (AVNRT)的电生理机制基本明确 ,射频消融方法肯定 ,但仍存在一些问题值得探讨。笔者分析探讨了以下几个方面 :①慢径消融还是快径消融 ;②AVNRT消融中出现交界性心动过速 (JT) ;③AVNRT慢径消融终点与复发率问题 ;④疑难AVNRT的射频消融 ;⑤消融中慢径阻断的判断指标 ;⑥自发而未诱发的AVNRT的射频消融。希望能对AVNRT的射频消融有一个更明确的认识 相似文献
8.
经导管射频消融改良房室结治疗房室结折返性心动过速 总被引:1,自引:0,他引:1
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。 相似文献
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射频消融慢径治疗房室结折返性心动过速术后晚期完全性房室阻滞 总被引:4,自引:1,他引:4
目的 观察选择性消融慢径术后的晚期完全性房室阻滞。方法 对1125例房室结折返性心动过速患者,采用下位法射频消融房室结慢径。结果 9(0.8%)例患者分别在术后第2、3和17天发生完全性房室阻滞,其中8例在消融术中有一过性完全性房室阻滞。平均随访2年.8倒的完全性房室阻滞持续存在,1例为间歇性;均无心动过速发作。结论慢径消融过程中一过性完全性房室阻滞可作为术后发生晚期完全性房室阻滞的先兆,术后应严密监测心电图。凝固性坏死灶外周损伤区的炎症反应是导致晚期完全性房室阻滞的可能机制。 相似文献
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目的:初步探讨射频改良房室结双径路的能量,房室传导阻滞发生率,初步手术成功率和复发率。方法:自1998年1月至2000年6月,对20例(女14例,男6例),平均年龄(43.4±17.1)岁频发房室结折返性心动过速(AVNRT)患者,采用射频消融能量从5W低能量开始,无效则按每5W逐渐递增,限定最大能量为30W进行消融慢径改良房室结功能。结果:20例患者全部改良成功,平均释放能量5~30W,平均(17.6±7.2)W,术后平均4~30个月随访,无1例发生房室传导阻滞并发症,其中1例术后2个月复发AVNRT,经再次射频消融慢径改良房室结功能成功。结论:采用低能量射频消融改良房室结功能,疗效满意,对减少房室传导阻滞并发症有益。 相似文献
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射频消融慢径后心动过速复发与房室结电生理特性变化的关系 总被引:2,自引:1,他引:2
为揭示房室结折返性心动过速(AVNRT)复发的机制,对45例射频消融治疗成功的慢-快型AVNRT患者在消融术前、术后即刻及术后逾三个月行电生理检查。结果10例复发(复发组)。复发组术前心房早搏刺激时的最大心房-His束间期(A2H2max)较非复发组明显延长(413±60msvs311±110ms,P<0.01);两组术后即刻A2H2max较术前均明显缩短(P均<0.01);术后三个月复发组的A2H2max较术后即刻明显延长(356±93msvs298±96ms,P<0.05),非复发组则有进一步缩短趋势,两组术后三个月的A2H2max比较有显著性差异(356±93msvs222±73ms,P<0.005);非复发组术后三个月A2H2max较术前明显缩短(222±73msvs311±110ms,P<0.01),房室结前传文氏周期及有效不应期较术前明显延长(405±91msvs366±84ms,332±75msvs269±63ms,P<0.01及<0.0001),复发组消融术前后比较差异则无显著性。结果提示部分AVNRT复发可能与其房室结本身电生理特性有关,基础状态下A2H2max长的患者心动过速更易复发。 相似文献
12.
JEFFREY E. OLGIN M.D. PHILIP URSELL M.D. ANN K. KAO M.D. MICHAEL D. LESH M.D. 《Journal of cardiovascular electrophysiology》1996,7(7):625-631
Pathology of Slow Pathway Ablation. Introduction : AV nodal reentrant tachycardia is routinely cured using radiofrequency catheter ablation techniques. However, there remains controversy as to whether the reentrant circuit for this tachycardia exists solely in the AV node or whether perinodal atrial tissues are vital to the circuit. In addition, the effects of radiofrequency ablation of the slow pathway of AV nodal reentrant tachycardia on the AV node are not known. We examined an autopsy specimen to determine the anatomical location and extent of AV nodal damage of radiofrequency slow pathway ablation for cure of AV nodal reentrant tachycardia.
Methods and Results : A 64-year-old woman with confirmed AV nodal reentrant tachycardia underwent a successful "slow pathway" AV modification with a single radiofrequency application. Five months after the procedure, the patient died from a spontaneous intracranial hemorrhage. Postmortem gross pathological examination of the heart was performed. The heart was then sectioned and stained for histologic examination. On gross examination, a pale lesion 0.5 cm in diameter was seen on the endocardial surface adjacent to the tricuspid annulus. approximately 0.85 cm anterior to the coronary sinus os and 1.15 cm from the apex of the triangle of Koch where the AV node resides. Histologic examination revealed a right atrial lesion composed of connective tissue and fat. The compact AV node and surrounding transitional cells were unaffected histologically, with normal atrial cells lying between the AV node and the lesion.
Conclusion : Ablation of the slow pathway to cure AV nodal reentrant tachycardia does not produce any gross or histologic damage to the AV node, suggesting that the AV nodal reentrant circuit does not exist in its entirety in the AV node. 相似文献
Methods and Results : A 64-year-old woman with confirmed AV nodal reentrant tachycardia underwent a successful "slow pathway" AV modification with a single radiofrequency application. Five months after the procedure, the patient died from a spontaneous intracranial hemorrhage. Postmortem gross pathological examination of the heart was performed. The heart was then sectioned and stained for histologic examination. On gross examination, a pale lesion 0.5 cm in diameter was seen on the endocardial surface adjacent to the tricuspid annulus. approximately 0.85 cm anterior to the coronary sinus os and 1.15 cm from the apex of the triangle of Koch where the AV node resides. Histologic examination revealed a right atrial lesion composed of connective tissue and fat. The compact AV node and surrounding transitional cells were unaffected histologically, with normal atrial cells lying between the AV node and the lesion.
Conclusion : Ablation of the slow pathway to cure AV nodal reentrant tachycardia does not produce any gross or histologic damage to the AV node, suggesting that the AV nodal reentrant circuit does not exist in its entirety in the AV node. 相似文献
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隐匿性拖带时起搏后间期与慢径消融成功靶点的关系 总被引:2,自引:0,他引:2
评价应用隐匿性拖带方法对准确靶点消融的有效性及探讨常规慢径靶点部位与房室结折返性心动过速(AVNRT)折返环的关系。可反复诱发的持续性典型AVNRT的患者 34例 ,消融导管在后或中间隔标测到A/V≤ 0 .5处 ,然后诱发心动过速 ,在高位右房 (HRA)和冠状窦口 (CSO)超速起搏产生隐匿性拖带 ,并按常规方法进行慢径消融。比较隐匿性拖带时靶点部位起搏后间期与心动过速周长的差值 (PPI-TCL值 )在成功靶点与不成功靶点区别。结果 :HRA超速起搏发生隐匿性拖带时 ,His束记录部位A波均为逆向夺获。而CSO超速起搏拖带时 ,32例His束记录部位A波为顺向夺获 ,另 2例为逆向夺获。在这 32例中共记录 5 4个靶点 ,成功靶点的PPI-TCL值明显小于不成功靶点 (12 .4± 5 .8msvs 32 .1± 18.6ms,P <0 .0 1)。PPI-TCL值≤ 2 0ms对靶点成功消融的敏感性和特异性分别为 84%、81%。结论 :本研究提示常规慢径消融成功部位作为房室结外的后部延伸组织参与组成AVNRT折返环或距其非常近。在可持续发作和诱发的AVNRT患者中 ,CSO部位起搏拖带顺向心房夺获时 ,靶点部位测出的PPI-TCL值≤ 2 0ms,可作为一种新的慢径路电生理定位消融方法 相似文献
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评价快速心房起搏时最快 1∶1房室传导的SV间期 (SV间期 )与 1∶1房室传导的最短S1S1间期 (SS间期 )的比值 (SV/SS)在房室结折返性心动过速 (AVNRT)慢径消融中的应用 ,将AVNRT分为房室结功能曲线连续组 (Ⅰ组 ,10例 )及房室结功能曲线不连续组 (Ⅱ组 ,17例 )测量心房分级递增刺激时的SS间期与SV间期及SV/SS ,并进行消融前、后和组间比较。结果显示 ,两组消融后SV间期较消融前明显缩短 (Ⅰ组 :2 2 1.0± 2 2 .3vs 35 7.0± 43.7ms;Ⅱ组 :2 0 2 .1± 30 .6vs 379.4± 44 .2ms,P均 <0 .0 5 ) ;消融前后SS间期无明显变化 (Ⅰ组 :310 .0± 40 .6vs 30 8.0± 36 .8ms;Ⅱ组 :332 .9± 48.1vs 336 .5± 6 2 .3ms) ;两组中所有患者消融前SV/SS比值均 >1,而消融后SV/SS比值均 <1。结论 :SV/SS可作为慢径消融成功终点的辅助观察指标之一 ,尤其对于房室结传导曲线呈连续性者 ,使用此方法可简便地观察消融终点 ,增加消融的目的性。 相似文献
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房室结改良时发生完全性房室阻滞的特征性心电改变 总被引:10,自引:3,他引:7
探讨经导管射频消融 (RFCA)治疗房室结折返性心动过速 (AVNRT)时发生完全性房室阻滞 (Ⅲ度AVB)前的特征性心电改变。回顾分析自 1996年 1月至 1999年 12月RFCA治疗AVNRT放电过程有完整心内电图记录者 486例。放电过程中有室房 (VA)阻滞、快速交界心律 (≥ 16 0bpm)和 /或房室 (AV)阻滞称为特征性心电改变。Ⅰ组 387例 ,任何一次放电过程中无特征性心电改变 ;Ⅱ组 99例 ,有一次或一次以上放电过程中有特征性心电改变。Ⅱ组中有特征性心电改变的放电共 316次 ,即刻停止放电组 (Ⅱa组 ) 2 19次 ,指发现特征性心电改变后 2s以内停止放电 ;延迟停止放电组 (Ⅱb组 ) 97次 ,指发现特征性心电改变 2s后停止放电。结果 :①AVNRT消融总成功率 97.9%(4 76 /4 86 ) ,永久性Ⅲ度AVB 0 .41% (2 /4 86 )。②特征性心电改变中VA阻滞占 72 .5 % (2 2 9/316 )、快交界心律占2 0 .6 % (6 5 /316 )、AV阻滞占 7.0 % (2 2 /316 )。③Ⅲ度AVB(包括一过性和永久性 )发生率为 2 .3% (11/4 86 ) ,其中Ⅰ组为 0 (0 /387)、Ⅱ组为 11.1% (11/99) ,P <0 .0 0 0 1。④Ⅱa组Ⅲ度AVB发生率为 0 .9% (2 /2 19)、Ⅱb组Ⅲ度AVB发生率为 9.3% (11/97) ,P <0 .0 0 1。RFCA改良房室结治疗AVNRT时Ⅲ度AVB均发生在特征性心电改变之后 ,发现特征? 相似文献
16.
探讨快 慢型房室结折返性心动过速 (AVNRT)射频消融治疗的方法学。 7例快 慢型AVNRT患者 ,在心动过速发作时 ,寻找慢径最早心房出口作为靶点行射频消融治疗。6例消融成功。与冠状静脉窦口 (CSp)相比 ,成功靶点A波提前程度平均为 9.8± 1.3ms。手术时间 87± 2 4min ,X线曝光时间 2 7± 12min ,无并发症 ,随访无 1例复发。结论 :激动标测寻找最早心房出口点作为消融靶点 ,是射频消融治疗快 慢型AVNRT安全有效的方法 相似文献
17.
Pseudo-Pacemaker Syndrome Following Inadvertent Fast Pathway Ablation for Atrioventricular Nodal Reentrant Tachycardia 总被引:2,自引:0,他引:2
YOU HO KIM M.D. SEAN O'NUNAIN M.D. TOM TROUTON M.D. GUILLERMO SOSA-SUAREZ M.D. ROBERT A. LEVINE M.D. HASAN GARAN M.D. JEREMY N. RUSKIN M.D. 《Journal of cardiovascular electrophysiology》1993,4(2):178-182
Pseudo-Pacemaker Syndrome After AV Nodal Ablation. Atrioventricular nodal reentrant tachycardia that is refractory to drug treatment has recently been treated with radiofrequency catheter ablation. In this case report we describe a patient with atrioventricular nodal reentrant tachycardia in whom radiofrequency ablation of slow pathway was attempted, with inadvertent damage to the fast pathway. The patient developed marked first-degree atrioventricular block associated with symptoms mimicking pacemaker syndrome. 相似文献
18.
JÜRGEN TEBBENJOHANNS M.D. DIETRICH PFEIFFER M.D. BURGHARD SCHUMACHER M.D. WERNER JUNG M.D. MATTHIAS MANZ M.D. BERNDT LÜDERITZ M.D. 《Journal of cardiovascular electrophysiology》1995,6(9):711-715
Influence of Slow Pathway Ablation on Atrial Fibrillation. Introduction : The mechanisms whereby radiofrequency catheter modification of AV nodal conduction slows the ventricular response are not well defined. Whether a successful modification procedure can be achieved by ablating posterior inputs to the AV node or by partial ablation of the compact AV node is unclear. We hypothesized that ablation of the well-defined slow pathway in patients with AV nodal reentrant tachycardia would slow the ventricular response during atrial fibrillation.
Methods and Results : In 34 patients with dual AV physiology and inducible AV nodal reentrant tachycardia, atrial fibrillation was induced at baseline and immediately after successful slow pathway ablation and at 1-week follow-up. The minimal, maximal, and mean RR intervals during atrial fibrillation increased from 353 ± 76,500 ± 121, and 405 ± 91 msec to 429 ± 84 (P < 0.01), 673 ± 161 (P < 0.01), and 535 ± 98 msec (P < 0.01), respectively. These effects remained stable during follow-up at 1 week. The AV block cycle length increased from 343 ± 68 msec to 375 ± 60 msec (P < 0.05) immediately and to 400 ± 56 msec (P < 0.01) at 1-week follow-up. The effective refractory period of the AV node prolonged from 282 ± 83 msec to 312 ± 89 msec and to 318 ± 81 msec after 1 week (P < 0.05), respectively.
Conclusion : This study shows a decrease in ventricular response to pacing-induced atrial fibrillation after ablation of the slow pathway in patients with AV nodal reentrant tachycardia. Since the AV nodal conduction properties could be defined, this study supports the hypothesis that the main mechanism of AV nodal modification in chronic atrial fibrillation is caused by ablation of posterior inputs to the AV node. 相似文献
Methods and Results : In 34 patients with dual AV physiology and inducible AV nodal reentrant tachycardia, atrial fibrillation was induced at baseline and immediately after successful slow pathway ablation and at 1-week follow-up. The minimal, maximal, and mean RR intervals during atrial fibrillation increased from 353 ± 76,500 ± 121, and 405 ± 91 msec to 429 ± 84 (P < 0.01), 673 ± 161 (P < 0.01), and 535 ± 98 msec (P < 0.01), respectively. These effects remained stable during follow-up at 1 week. The AV block cycle length increased from 343 ± 68 msec to 375 ± 60 msec (P < 0.05) immediately and to 400 ± 56 msec (P < 0.01) at 1-week follow-up. The effective refractory period of the AV node prolonged from 282 ± 83 msec to 312 ± 89 msec and to 318 ± 81 msec after 1 week (P < 0.05), respectively.
Conclusion : This study shows a decrease in ventricular response to pacing-induced atrial fibrillation after ablation of the slow pathway in patients with AV nodal reentrant tachycardia. Since the AV nodal conduction properties could be defined, this study supports the hypothesis that the main mechanism of AV nodal modification in chronic atrial fibrillation is caused by ablation of posterior inputs to the AV node. 相似文献
19.
A波延迟电位在慢径消融靶点定位中的应用 总被引:3,自引:1,他引:2
为了探讨A波延迟电位在慢径消融靶点定位中的应用价值 ,对传统下位法和A波延迟电位引导下的慢径消融两组病例的靶点的电生理特征进行了研究。结果 :延迟电位引导下的慢径消融在提高成功率、减少试放电方面明显优于下位法。有效靶点的突出特征是A波宽度 >6 8ms、A波终末具延迟电位 ,A/V比例不能作为预测靶点的指标。A波延迟电位有四种形态 ,分别为单弓状延迟电位、双弓状延迟电位、穗状电位及A波终末的高频电位 ,其中以前两种最为常见。当程序刺激遇快径不应期而经慢径传导时 ,靶点正传的A波更加延迟 ,逆传A波更加领先是成功靶点的特征。结论 :在慢径消融的靶点定位中应用A波延迟电位和程序刺激可提高成功率、减少盲目性 ,A波延迟电位引导慢径消融方法优于传统的消融方法慢径消融方法优于传统的消融方法 相似文献
20.
选择性消融逆传快径治疗典型房室结折返性心动过速 总被引:3,自引:2,他引:1
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。 相似文献