异丙肾上腺素对射频消融房室结折返性心动过速疗效…

地消融房室结慢径的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）从未能诱发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）和异丙肾上腺素评价，其中９例既有吉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     

房室结折返性心动过速慢径消融终点与临床疗效关 …

６２例慢－快型房室结折返性心动过速（ＡＶＮＲＴ）患者接受慢径消融治疗，评价Ａ型终点（阻断慢径且不再诱发ＡＶＮＲＴ）、Ｂ型终点（保留慢径前传但不再诱发ＡＶＮＲＴ和心房回波）和Ｃ型终点（保贸慢径且能诱发１～３个心房回波）对房室传导功能的影响及与ＡＶＮＲＴ复发的关系。结果：（１）消融后７７．４％（４８例）；１７．７％（１１例）和４．８％（３例）的病人分别达Ａ、Ｂ和Ｃ型终点；（２）消融后Ａ型终点病人的房室     

异丙肾上腺素在射频导管消蚀房室结折返性心动过速中的意义（摘要）

异丙肾上腺素在射频导管消蚀房室结折返性心动过速中的意义（摘要）胡大一杨新春葛永贵商丽华马长生３４例房室结折返性心动过速（ＡＶＮＲＴ）患者接受异丙肾上腺素（异丙肾）诱发试验，其中２０例在消蚀前电生理检查诱发ＡＶＮＲＴ阴性，静滴异丙肾（１～３μｇ／ｍｉｎ...     

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     

射频消融房室结慢径对诱发Ⅰ型房扑的影响

目的 观察射频消融房室结慢径对诱发Ⅰ型房扑（ＡＦＬ）的影响，分析这２种心和人常之间的关系和探讨房室结慢径的本质。方法 ２１例房室结折返性心动过速（ＡＶＮＲＴ）患，分别于射频消融前后行心房程序电刺激恨ＡＦＬ。结果 慢径消融前ＡＦＬ恨率为９０．４８％，慢径消融后 诱发率为３８．１０％，较消融前明显降低。结论右心房后下部组织是ＡＶＮＲＴ和ＡＦＬ折返环路的共同部分，慢径是右心房后下部缓慢传导组织向房室结     

房室结折返性心动过速患者房室结功能曲线连续 …

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６６％（２３／３５）。Ⅰ组房室结前传有效不应期（ＥＲＰ－ＡＶＮ）消融前后无显著变化（２１８     

快-慢型房室结折返性心动过速的电生理特征和射频消融治疗

报道８例快－慢型房室结折返性心动过速（ＡＶＮＲＴ）的电生理特征及射频消融治疗。其中３例为慢－快型ＡＶＮ－ＲＴ射频消融改良慢径后出现的快－慢型ＡＶＮＲＴ。８例均经消融慢径而成功终止心动过速。平均放电次数３±１．１次、平均放电时间１２０±３０．４ｓ、平均放电功率３０±１１Ｗ。随访６～２４个月，无复发。快－慢型ＡＶＮＲＴ具有以下临床电生理特征：①快径不应期短、慢径不应期长。②心内电刺激无房室结双径路现象。③心动过速能由心房刺激诱发。④心动过速时ＡＨ间期＜ＨＡ间期，冠状窦近端Ａ波最提前。熟悉快－慢型ＡＶＮＲＴ的电生理特征，对于鉴别房性心动过速及右后间隔旁道参与的房室折返性心动过速十分重要，也是指导快－慢型ＡＶＮＲＴ射频消融成功的关键。     

心房起搏法在射频消融房室结折返性心动过速中的应用

将射频消融治疗的９４例房室结折返性心动过速（ＡＶＮＲＴ）病人按心房起搏法和常规法进行分组（分别为３９及５５例），回顾性比较两组病人的消融治疗结果，以评价这两种方法在射频消融治疗ＡＶＮＲＴ中的安全性、成功率和复发率。随访１０．８±４．５个月，总成功率为９６．８％、复发率为２．１％。与常规组相比，起搏组有效放电时间明显延长（１４５±３８ｓｖｓ８２±２６ｓ，Ｐ＜０．０１）、慢径阻断成功率高（６１．５％ｖｓ４０．０％，Ｐ＜０．０１）、一过性房室阻滞发生率低（２．６％ｖｓ１２．７％，Ｐ＜０．０５），但各种类型的永久性房室阻滞发生率和复发率无显著性差异（Ｐ＞０．０５）。表明ＡＶＮ－ＲＴ消融术中采用心房起搏法较常规法更为安全有效。     

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。     

射频导管消融治疗房室结折返性心动过速中较难病例的电生理特点

目的：明确射频导管消融治疗房室结折返性心动过速（ＡＶＮＲＴ）中较难病例的电生理特点。方法：７２例行慢径射频导管消融的慢—快型ＡＶＮＲＴ病人中１１例（１５％）成功射频导管消融的放电次数超过２０次或总放电时间超过２００秒被定义为较难病例（较难组），其余的为非较难病例（非较难组）６１例（８５％）。结果：较难组１１例中有７例（６４％）短心房—希氏束间期（≤６０ｍｓ），而非较难组６１例中１４例（２３％）短心房—希氏束间期（≤６０ｍｓ，Ｐ＜０．０５）；较难组１１例中８例（７３％）短房室结逆传文氏周期（≤２８０ｍｓ）；非较难组５７例（６１例中有４例因心室刺激反复诱发心动过速不能测得逆传文氏周期）中有１５例（２６％）具有短房室结逆传文氏周期（≤２８０ｍｓ，Ｐ＜０．０１）。７２例中５５例（７６％）具有房室结前传不连续曲线。房室结前传曲线有多次“跳跃”在较难组１１例中有７例（６４％）病人，在非较难组中有１２例病人（２０％，Ｐ＜０．０１）。结论：短心房—希氏束间期、短房室结逆传文氏周期和前传曲线多次“跳跃”的病人在较难组所占的百分率明显高于非较难组，有显著差异。     

Role of the AV node and adrenergic stimulation in initiation of fascicular and atrioventricular nodal tachycardias--a case report

Fascicular tachycardia is an uncommon form of left ventricular tachycardia in young patients with normal heart. Ventriculo-atrial conduction during VT is usually absent. Retrograde conduction was observed in a 14-year old boy with left posterior fascicular VT (LPF-VT) triggered by exercise. During isoproterenol infusion, atrial stimulation induced a cascade of arrhythmias--echo, pair or runs of AVNRT and fascicular tachycardia triggered by fascicular beats. Also, during infusion LPF-VT was initiated spontaneously. After successful ablation of VT, sustained typical AVNRT was inducible. Finally, ablation of slow pathway of AV node was performed. After ablation,no arrhythmia was inducible following isoproterenol and exercise.     

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。     

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。     

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.     

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.     

房室结折返性心动过速射频消融术后复发机制探讨

目的: 探讨房室结折返性心动过速射频消融术后复发原因。方法: 对356 例房室结折返性心动过速患者射频消融术后进行随访,回顾性分析其电生理资料。结果: 356例中10例复发,复发率2.8%,320例患者射频术后无心房回波,无跳跃现象,一直未复发;术后有心房回波无跳跃现象未诱发出室上速17例,其中3例复发;术后有跳跃及心房回波未诱发出室上速11例,其中5例复发;术后有跳跃无心房回波未诱发出室上速8例,2例复发。10例复发患者,第2次射频消融术后房室结不应期均较第1次术后延长,且与术前快径不应期差值明显减小,第2次射频消融术后随访至今（>9个月）,无1例复发。结论: 慢径残存是房室结折返性心动过速射频消融术后复发的主要原因。     

Conversion of typical to "atypical" atrioventricular nodal reentrant tachycardia after radiofrequency catheter modification of the atrioventricular junction.

Typical atrioventricular (AV) nodal reentry tachycardia (AVNRT) is characterized by anterograde activation over a slowly conducting pathway and by retrograde activation through a rapidly conducting pathway. Preliminary reports suggest that radiofrequency catheter modification can eliminate typical AVNRT while preserving anterograde conduction. Radiofrequency catheter modification was used to treat 88 patients with typical AVNRT. After baseline electrophysiologic evaluation, the ablation catheter was positioned proximal and superior to the site of maximal His deflection. Radiofrequency energy was applied until there was significant attenuation of retrograde conduction, and elimination of AVNRT inducibility. Eighty-one patients were successfully treated and form the basis of this report. A new paroxysmal supraventricular tachycardia with RP greater than PR interval was induced at electrophysiologic testing after successful ablation in 9 patients (11%). Mean atrial-His activation time was 140 +/- 31 ms, and the ventriculoatrial activation time was 170 +/- 46 ms. This arrhythmia was induced only with ventricular pacing during isoproterenol infusion and appeared to be mediated by AV nodal reentry. New retrograde dual AV nodal physiology after modification was more frequent in patients with atypical tachycardia than in those without (4 of 9 vs 2 of 72; p less than 0.0001). Although none of the patients were treated, only 1 of 9 had an episode of spontaneous atypical tachycardia during a mean follow-up of 12 months. Results of this study confirm that typical AVNRT can be rendered noninducible without the complete destruction of reentrant pathways. Because induction of "atypical" AVNRT was not predictive of spontaneous arrhythmia recurrence, it should not be an indication for additional ablation sessions or long-term drug therapy.     

房室结改良术终点与复发率的关系

为探讨房室结改良术成功后不同电生理终点对复发率的影响，观察了８０例房室结改良术患者复发情况。其中双径现象消失（Ａ组）５１例；仍有双径现象，但无心房回波（Ｂ组）２１例；有双径现象，且有１个心房回波（Ｃ组）８例。消融成功后观察３０ｍｉｎ，急性复发４例（５．８％）；术后随访１４．７±５．６（６～３９）个月慢性复发３例（３．８％），共复发７例（８．８％）。７例中，Ａ组与Ｂ组各２例、Ｃ组３例，复发率分别为３．９％、９．５％、３７．５％。其中Ａ组与Ｃ组比较复发率差异非常显著（Ｐ＜０．０１），其余差异无显著性（Ｐ＞０．０５）。此结果表明，选用三种终点中的任何一种，术后大多数患者都未复发。而为了降低复发率，除了消融成功后至少应观察３０ｍｉｎ以消除急性复发外，在技术成熟的单位，可力争以双径现象消失为改良术终点。     

房室结折返性心动过速慢径消融终点与临床疗效关系探讨

62例慢-快型房室结折返性心动过速（AVNRT）患者接受慢径消融治疗,评价A型终点（阻断慢径且不再诱发AVNRT）、B型终点（保留慢径的传但不再诱发AVNRT和心房回波）和C型终点（保留慢径且能诱发1～3个心房回波）对房室传导功能的影响及与AVNT复发的关系。结果：①消融后77．4％（48例）;17．7％（11例）和4．8％（3例）的病人分别达A、B和C型终点;②消融后A型终点病人的房室传导功能明显改善,B、C型变化不明显;③术后3～7天经食管电生理复查,A型终点AVNRT的再诱发率为2．1％（1例）、B型为18．2％（2例）、C型为33．3％（1例）;④41例病人保持随访8．9±7．1个月,A型终点AVNRT复发率为4．9％,B、C型为28．6％。结果揭示AVNRT慢径消融中大多数病人可达到A型终点,且彻底阻断慢径后房室传导功能明显改善,AVNRT的近期和远期复发率明显低于B到和C型终点。     

Effects of ablation, digitalis, and beta-blocker on dual atrioventricular nodal pathways and conduction during atrial fibrillation

INTRODUCTION: Modification of AV nodal conduction by radiofrequency ablation (RFA) results in a variable reduction in heart rate during atrial fibrillation (AF). Using AF induced in patients with dual AV nodal pathways as a model, we tested the effect of additional treatment with digitalis (ouabain) and beta-blocker (esmolol). METHODS AND RESULTS: Ten patients were randomized to control (group I) and studied only before ablation. AF was induced in 30 patients before and after slow pathway ablation (group II). Mean ventricular cycle lengths (AF CLmean) were recorded. Slow pathway conduction was eliminated after ablation in 10 patients (group IIA), whereas slow pathway conduction was still present in 20 patients (group IIB). Compared to pre-RFA there was a 10% increase in AF CLmean post-RFA (P < 0.01). During isoproterenol infusion the increase was 8% (P = NS). Adding digitalis and beta-blocker during isoproterenol infusion increased AF CLmean by 75% (95% in group IIA) compared to 36% in group I (P < 0.001 II vs I). CONCLUSION: Slow pathway ablation reduces ventricular rate during AF. Addition of digitalis and beta-blocker during isoproterenol infusion significantly decreases ventricular rate after ablation compared to the control group. The finding suggests that beta-blocker has significant effects on fast AV nodal pathway conduction during induced AF with isoproterenol infusion.