Ⅲ度房室传导阻滞伴房室结折返性心动过速一例

完全性房室(室房)传导阻滞者合并房室结内折返性心动过速实属罕见。房室结折返性心动过速其折返环主要在房室结和/或周围组织,心房、心室并不参与折返性心动过速,因此,在房室结折返性心动过速时,偶尔可发现室房2:1传导,甚至房室2:1传导,这也证明了心房、心室不参与折返性心动过速。本例患者心脏电生理检查显示:房室结折返时经His束下传到心室,形成房室结折返性心动过速,由于房室结-心房阻滞,所以才伴房室(室房)分离,即Ⅲ度房室传导阻滞。鉴于该患者既有心动过缓又有心动过速,治疗上需综合考虑。在植入起搏器之前,先行房室结改良术,然后再植入双腔起搏器。     

慢快型房室结内折返性心动过速伴下部共同径路2:1房室传导阻滞

慢快型房室结内折返性心动过速(AVNRT)在临床上较为常见。但房室结内形成的折返在下部共同径路存在传导障碍,而出现2∶1房室传导阻滞较为少见。我们在行食管电生理和心内电生理检查时遇见6例,现报道如下。资料和方法1.对象。1995年5月至2002年2月来院心内科门诊和住院患者6例,男性4例,女性2例,年龄34~65岁。均有心动过速发作史3～10年,发作时的体表心电图已确诊为房室结内折返性心动过速,准备行射频导管消融术。在术前和/或术中的检查中发现慢快型房室结内折返性心动过速,发作时呈2∶1房室传导阻滞。2.方法。以习用的食管电生理和心内电生…     

房室结双径路传导所致特殊心电图改变

为了解房室结双径路传导所致的较为特殊心电图改变,对食管电生理检查中发现的双径路传导和房室结内折返性心动过速进行分析。发现:(1)双径路传导可以造成不同程度的假性房室传导阻滞,(2)双径路同步1:2房室传导可造成交接区和室性心律失常的假象,(3)在房室结内折返性心动过速发生上部和下部共同径路传导阻滞时又可使心电图表现复杂化。上述改变对进一步认识房室结双径路传导与心律失常的关系有重要意义,能显著提高对房室结双径路传导的正确诊断。     

1∶2房室传导诱发房室结非折返性心动过速1例

基于动态心电图及食管电生理检查,以心内电生理检查为金标准,确诊1例为1∶2房室传导诱发房室结非折返性心动过速,经射频消融改良慢径后,最终根治心动过速.     

房室双旁道的食管心脏电生理特征

目的：探讨房室双旁道食管心脏电生理检查的特征性改变。方法：对14例经射频导管消融术证实的房室双旁道的食管心脏电生理检查作回顾性分析。结果：10例房室双旁道的电生理特征为：（1）心房起搏时显示两种不同的预激图形和／或特殊类型室性融合波群，经食管心房起搏有利于显现左侧旁道。（2）诱发出两种逆向型房室折返性心动过速，由两条旁道形成折返环路。（3）顺向型房室折返性心动过速时，出现两种不同的R－P^-间期和P^-波或房性融合波。（4）排除房室结双径路后，逆向型房室折返性心过速的频率快于顺向型房室折返性心动过速。（5）预激旁道的部位与顺向型房室折返性心动过速时P^-波提示的部位不同。（6）双旁道隐匿性传导是造成其中一条旁道丧失传导功能的重要因素之一。另4例未能表现出上述电生理特征，其中右侧隐性旁道合并左侧隐匿性旁道1例，右侧隐匿性双旁道1例，左侧隐匿性双旁道2例。结论：食管心脏电生理检查能够确诊大部分的房室双旁道，采用多导联同步记录及在房室折返性心动过速时仔细分析电生理表现有助于揭示房室双旁道。     

经食管心脏电生理检查误诊房室折返性心动过速的不典型房室结折返性心动过速的特点及分析

目的探讨食管电生理检查中被误诊为房室折返性心动过速的不典型的慢快型房室结折返性心动过速的特点。方法回顾性分析5例误诊为房室折返性心动过速患者的食管电生理及心内电生理资料。结果 5例患者在食管电生理检查S1S2程控期前刺激中,均未观察到S2-R间期有跳跃性延长,心动过速的R-P-EB间期70ms;逆行P-波在V1导联直立,下壁导联倒置;食管电生理诊断为左后间隔隐匿性旁道参与的房室折返性心动过速。心内电生理诊断为慢快型房室结折返性心动过速,并成功消融慢径路。结论部分R-P-EB间期70ms的不典型慢快型房室结折返性心动过速食管电生理特点与后间隔隐匿性旁道参与的房室折返性心动过速类似,必要时需心内电生理检查加以明确。     

房室结折返性心动过速室房传导的规律

通过窄 QRS心动过速的心电图 RP′间期及心内电图VA间期变化 ,探讨房室结折返性心动过速 (atrioventriculanodal reentrant tachycardia,AVNRT)室房传导的规律性。　　资料和方法　选择对象为经心内电生理检查及射频消融治疗证实为房室结双经路慢 -快型折返性心动过速的 46例患者 ,男性 2 0例 ,女性 2 6例 ,平均年龄 (4 4± 15 )岁。 46例患者 ,窦性心律时心电图无异常 ,心动过速时呈窄 QRS波 ,QRS时限 <0 .11s,伴 1∶ 1的室房激动关系 ,心动过速时记录体表心电图及希氏束 (HBE)及冠状静脉窦近端 (CS9～10 )心内电图来观察 RP′间…     

房室结双径路伴房室结折返性心动过速的室房传导研究

<正> 随着临床电生理技术的完善和射频消融治疗快速心律失常的广泛应用,要求术者对不同折返途径的室房传导有更深入的了解,本文旨在研究房室结双径路(DAVNP)伴房室结折返性心动过速(AVVRT)室房(V-A)传导的特征,并以房室旁道伴房室折返性心动过速(AVRT)作为对照.     

快频率依赖性室房逆传左侧隐匿性房室旁道参与的心动过速及射频导管消融

目的探讨快频率依赖性室房逆传特性左侧隐匿性房室旁道的电生理特点及射频消融。方法对8例心电图显示窄QRS波群心动过速的患者行电生理检查,分析房室、室房传导情况、心动过速特点、旁道定位,并行射频消融。结果8例患者均证实存在快频率依赖性室房逆传特性左侧隐匿性旁道,在较慢频率起搏右心室时旁道逆传发生阻滞,而以中等频率起搏时表现为间断旁道逆传,较快频率起搏时才表现为旁道1：1传导且均诱发了房室折返性心动过速,于快频率心室刺激下标测消融靶点,消融均获成功。结论左侧隐匿性房室旁道有时可发生快频率依赖性室房逆传现象,并伴发房室折返性心动过速,在射频消融中需注意分辨,以免漏诊。     

预激综合征1:2房室传导及其变异

目的 探讨预激综合征患者发生l：2房室传导时的电生理表现及形成机制。方法 分析在心内法和食管法心脏电生理检查中发现的3例预激综合征1：2房室传导和1例1：2室房传导现象。结果 电生理改变为：①心房期前收缩偶联间期缩短到一定程度后才出现两次心室激动，QRS波群第1次呈预激型，第2次呈束支传导阻滞型，R2与R2′波之间无P波；②心房期前收缩偶联间期缩短10ms，出现突然延长的S2-R2′间期，表明存在房室结双径路传导；③房室结慢径路传导延缓程度不够，两条径路未形成足够的传导时间差，因激动无法脱离下部共同径路或心室肌不应期，致l：2房室传导被掩盖；④一次室性期前收缩后出现两次激动顺序一致的旁道逆传性心房激动，并诱发顺向性房室折返性心动过速。结论 ①预激综合征患者存在房室结双径路传导是引起传导显著缓慢、形成l：2房室传导的主要原因；②l：2房室传导较少见，是因为旁道与房室结的传导速度之差不够大，致沿房室结下传的激动难以脱离心室不应期。此外，旁道和房室结两条径路之间的隐匿性折返也是激动无法再次下传的重要原因；③出现显著晚于V波的H2波表明两条径路发生了同步传导，虽然未形成R2波，但可称为隐匿性l：2房室传导。     

房室结折返性心动过速伴2:1房室阻滞的机制初探

目的 本研究探讨电生理检查时诱发的房室结折返性心动过速（AVNRT）伴2:1AVB的机制和阻滞部位。方法 回顾分析电生理检查中遇到的9例AVNRT伴2:1AVB患者的资料。结果4例希氏束记录不全的不作分析,其余5例患者中,3例在阻滞的激动上见到H波,在发生AVNRT伴2:1AVB起始阶段出现H-V文氏传导阻滞伴LBBB或RBBB,另外2例在阻滞的激动上未见H波,但有一例2:1AVB过程中突然出现一次H-V3:1文氏传导阻滞。结论 电生理检查诱发的AVNRT伴2:1AVB可能是功能性的希-浦系统阻滞。     

Implications of 2:1 atrioventricular block during typical atrioventricular nodal reentrant tachycardia

Objective The effects of 2:1 AV block (AVB) on AV nodal reentrant tachycardia (AVNRT) remain to be elucidated. This study was performed to localize the site of 2:1 AVB and elucidate the effects of 2:1 AVB on typical AVNRT. Methods The His bundle (HB) electrograms during typical AVNRT with 2:1 AV block were reviewed in 24 patients. It was hypothesized that if 2:1 AVB at the HB or below changed tachycardia cycle length (TCL), the lower turnaround point of the reentrant circuit (RC) might be located within the HB and parts of the HB might be involved in the RC. Results A HB potential was absent in blocked beats during 2:1 AVB in four patients (supra-Hisian block), and the maximal amplitude of the HB potential in blocked beats was the same as that in conducted beats in four patients (infra-Hisian block), and was significantly smaller than that in conducted beats (0.1 ± 0.1 versus 0.5 ± 0.2 mV, P < 0.05) in 16 patients (intra-Hisian block). Eight patients (33%) with intra-Hisian block had a nearly identical prolongation of the H–A and A–A intervals in blocked beats (12 ± 3 and 13 ± 2 ms, respectively) with unchanged A–H intervals, while the remaining 16 patients (67%) exhibited invariable A–A and/or H–A intervals. Conclusion The site of 2:1 AVB during typical AVNRT was estimated to be at the HB or below in 83% of the cases. Two-to-one intra-Hisian block transiently prolonged TCL, possibly indicating involvement of the proximal HB in the RC in one-third of typical the AVNRT cases with 2:1 AVB.     

房室结双径路慢径消融时连续AV非1∶1比例与短暂房室传导阻滞的相关性

目的分析房室结双径路导管射频消融时出现连续AV非1∶1比例与房室传导阻滞(AVB)发生的相关性及放电导致AVB的特点,为消融时预防AVB提供思路与方法。方法回顾113例房室结双径路的导管消融电生理资料,分析放电时AV的比例、波幅比值及患者性别、年龄等因素与出现AVB的相关性。结果放电时出现连续AV非1∶1比例时,短暂AVB的发生率显著高于无AV非1∶1比例者(36.84%vs 0.52%,P<0.05)。靶点腔内心电图呈小A大V,A波较宽、碎裂,不带有H波,在此基础上放电是否出现AVB与AV波幅比值无关(P>0.05)。女性AVB的发生率高于男性(34.78%vs 6.82%,P<0.05)。随访中未见AVB发生及室上性心动过速复发。结论放电时出现连续AV非1∶1比例可能发生AVB,须立即停止放电;女性患者更易出现AVB。     

Electrophysiologic Characteristics and Radiofrequency Catheter Ablation in Atrioventricular Node Reentrant Tachycardia with Second-Degree Atrioventricular Block

Second-Degree AV Block During AVNRT. Introduction : Detailed electrophysiologic study of AV nodal reentrant tachycardia (AVNRT) with 2:1 AV block has been limited.
Methods and Results : Six hundred nine consecutive patients with AVNRT underwent electrophysiologic study and radiofrequency catheter ablation of the slow pathway. Twenty-six patients with 2:1 AV block during AVNRT were designated as group I, und those without this particular finding were designated as group II. The major findings of the present study were: (1) group I patients had better anterograde and retrograde AV nodal function, shorter tachycardia cycle length (during tachycardia with 1:1 conduction) (307 ± 30 vs 360 ± 58 msec, P < 0.001), and higher incidence of transient bundle branch block during tachycardia (18/26 vs 43/609, P < 0.001) than group II patients: (2) 21 (80.8%) group I patients had alternans of AA intervals during AVNRT with 2:1 AV block. Longer AH intervals (264 ± 26 vs 253 ± 27 msec, P = 0.031) were associated with the blocked beats. However, similar HA intervals (51 ± 12 vs 50 ± 12 msec, P = 0.363) and similar HV intervals (53 ± 11 vs 52 ± 12, P = 0.834) were found in the blocked and conducted beats; (3) ventricular extrastimulation before or during the His-bundle refractory period bundle could convert 2:1 AV block to 1:1 AV conduction.
Conclusions : Fast reentrant circuit, rather than underlying impaired conduction of the distal AV node or infranodal area, might account for second-degree AV block during AVNRT. Slow pathway ablation is safe and effective in patients who have AVNRT with 2:1 AV block.     

Noninvasive Diagnosis in Patients with Undocumented Tachycardias:

INTRODUCTION: Patients with symptoms suggestive of paroxysmal supraventricular tachycardia (PSVT) but no tachycardia documentation often undergo diagnostic electrophysiologic study. In dual AV node physiology with AV node reentrant tachycardia (AVNRT), the anterograde fast pathway is more sensitive than the slow pathway to the effects of adenosine. The purpose of the study was to test the hypothesis that adenosine can be used as a bedside test for the diagnosis of dual AV node physiology and hence for AVNRT. METHODS AND RESULTS: During electrophysiologic study, 37 patients without prior documentation but symptoms indicative for PSVT received incremental dosages of adenosine during sinus rhythm until second-degree or greater AV block was observed. Suggestive signs of dual AV node physiology on the surface ECG (sudden jump of PQ interval > or = 50 msec) were found in 13 (76%) of 17 patients with inducible AVNRT but in only 1 (5%) of the remaining patients (P < 0.01). In the AVNRT group, the maximal increase of the PQ interval between two beats was greater (88+/-45 msec) than in the remaining 20 patients (17+/-11 msec) (P < 0.01). CONCLUSION: Careful evaluation of surface ECG during administration of adenosine helps to identify patients prone to AVNRT. The adenosine test is a valuable noninvasive adjunct in patients with undocumented palpitations suggestive of PSVT.     

Atrioventricular nodal Reentrant Tachycardia with Atrioventricular Block

Atrioventricular block (AVB) during atrioventricular nodal reentrant tachycardia (AVNRT) has been well documented [1-4], although it is not a common phenomenon. The mechanism for the initiation and resolution of AVB during AVNRT have been postulated [2,4]. However, the site of AVB and its implication on the reentrant circuit in AVNRT is not clear. We illustrate two examples of AVNRT with AVB and offer further clarification on the site and mechanism of AVB.     

能量滴定法在慢径改良术中预防房室传导阻滞的作用研究

目的探讨“能量滴定法”在射频消融治疗房室结折返性心动过速术中对房室传导阻滞的预防作用。方法收集经射频消融术治疗的房室结折返性心动过速865例;消融过程采用“下位法+能量滴定法”。结果治疗成功率98.9%,复发率为2.08%,10例患者出现I°房室传导阻滞,无III°房室传导阻滞发生。靶点数≥5.0、有效靶点/总靶点<70%和累计消融能量(W*S)≥2300的患者房室传导阻滞的发生率明显增高(P<0.05),而复发率则无明显差异。结论射频消融术治疗房室结折返性心动过速减少累计消融能量、控制总靶点数和提高靶点有效率能有效减少房室传导阻滞的发生。     

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。     

Spontaneous transition of 2:1 atrioventricular block to 1:1 atrioventricular conduction during atrioventricular nodal reentrant tachycardia: evidence supporting the intra-Hisian or infra-Hisian area as the site of block

INTRODUCTION: The incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction during AV nodal reentrant tachycardia has not been well reported. Among previous studies, controversy also existed about the site of the 2:1 AV block during AV nodal reentrant tachycardia. METHODS AND RESULTS: In patients with 2:1 AV block during AV nodal reentrant tachycardia, the incidence of spontaneous transition of 2:1 AV block to 1:1 AV conduction and change of electrophysiologic properties during spontaneous transition were analyzed. Among the 20 patients with 2:1 AV block during AV nodal reentrant tachycardia, a His-bundle potential was absent in blocked beats during 2:1 AV block in 8 patients, and the maximal amplitude of the His-bundle potential in the blocked beats was the same as that in the conducted beats in 4 patients and was significantly smaller than that in the conducted beats in 8 patients (0.49 +/- 0.25 mV vs 0.16 +/- 0.07 mV, P = 0.007). Spontaneous transition of 2:1 AV block to 1:1 AV conduction occurred in 15 (75%) of 20 patients with 2:1 AV block during AV nodal reentrant tachycardia. Spontaneous transition of 2:1 AV block to 1:1 AV conduction was associated with transient right and/or left bundle branch block. The 1:1 AV conduction with transient bundle branch block was associated with significant His-ventricular (HV) interval prolongation (66 +/- 19 ms) compared with 2:1 AV block (44 +/- 6 ms, P < 0.01) and 1:1 AV conduction without bundle branch block (43 +/- 6 ms, P < 0.01). CONCLUSION: The 2:1 AV block during AV nodal reentrant tachycardia is functional; the level of block is demonstrated to be within or below the His bundle in a majority of patients with 2:1 AV block during AV nodal reentrant tachycardia, and a minority are possibly high in the junction between the AV node and His bundle.     

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.