室房逆传的再探讨

目的 探讨在体房室结无室房逆传或逆传功能明显低于房室顺传的机制。方法 对128例心脏介入性诊疗术患者，分别作心房、心室刺激，观察经房室结顺传及室房逆传的电生理特征。结果 除21例三度房室传导阻滞外，107例房室顺传文氏点大于150次／min；有经房室结室房逆传者12例（11．2％），其中室房逆传文氏点10例小于130次／min，2例为130次／min。95例（88．8％）及21例三度房室传导阻滞者均无室房逆传。结论 绝大多数在体房室结固有逆传功能明显低于房室顺传，或呈单向传导。房室旁道和／或房室结逆传快径路是室房逆传良好的主要原因及形成阵发性室上性心动过速等病症的根本机制。     

射频消融治疗具有快频率依赖性室房逆传特性的旁道

目的报道具有快频率依赖性室房逆传特性的房室旁道电生理检查及射频消融结果。方法4例患者,均有阵发性心悸史,且发作时心电图均显示为窄QRS波心动过速,按常规方法接受心脏电生理检查及射频消融治疗。结果4例均证实存在旁道的快频率依赖性室房逆传,且均诱发了房室折返性心动过速,室房逆传最早激动部位均为左房。于快频率心室刺激下标测消融靶点,消融均获成功。结论旁道的快频率依赖性传导为一种少见电生理现象,可伴发房室折返性心动过速。     

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.     

儿茶酚胺依赖性隐匿房室旁道一例

患者男性,45岁,因阵发性室上性心动过速入院。心内电生理检查为左侧隐匿性房室旁道(AP),在基础状态时,该AP既无前传也无逆传功能,但应用异丙肾上腺素后表现出了逆传功能,在持续静脉输注异丙肾上腺素情况下,完成射频消融术。     

房室折返性心动过速合并房室结双径现象

目的 分析射频消融术证实的房室帝道（ＡＰ）合并房室结双径（ＤＡＶＮＰ），以了解其电生理特点。方法 以食管心房调博及心内电生理检查，确诊室上速合并房室结双径１２例，并行射频消融枚。结果 ＡＰ合并ＤＡＶＮＰ占ＡＰ的１６．４％（１２／７３），多为陷匿性ＡＰ（１０／１２），其折返途径多为ＡＰ逆传（１０／１２），房室结单一径路前传，房室结快径道不应期及心动过速时ＲＰ’（ＶＡ）与ＲＰ意期，在食道电生理与心内电     

室房逆传的现代认识

<正>正常心脏的激动起源于窦房结,冲动以辐射状的方式先后激动右心房、房间隔及左心房,随之依次向下通过房室结、希氏束、束支及浦肯野纤维系统扩布到心室。如果起源于心室的激动逆行向上传导激动心房,则发生了室房逆传(Retrograde ventriculoatrial conduction,Retrograde VA conduction)现象。随着心电学及心电生理技术的发展,房室前传早已被广泛研究。1913年,Mines首次描述了室房逆传,此后心电学和心电生理学工作者对室房逆传的探索及研究已有一个世纪。室房逆传是房室折返性     

房室旁道间歇性逆传阻滞的探讨

为探讨房室旁道间歇性逆传阻滞的发生机制及临床意义,对房室旁道患者射频导管消融术中作腔内电生理检查,观察房室顺传和室房逆传功能及途径。结果显示２６１例中有７例（４例为隐匿性预激综合征）为旁道逆向（或双向）传导阻滞（２．７％）。尽管旁道间歇性逆传阻滞是一种少见现象,但由于旁道传导阻滞,无法对旁道进行定位及射频导管消融,因此了解旁道有无间歇性逆传阻滞,对射频导管消融治疗有临床意义。     

射频消融房室结慢径对老年人房室结电生理功能的影响

目的　分析和比较应用射频消融房室结慢径治疗房室结折返性心动过速对老年人和青年人房室结电生理功能的影响。方法　 76例仅患有慢 快型房室结折返性心动过速的患者分为两组 ,老年组 (≥ 6 0岁 ) 36例和青年组(14～ 4 5岁 ) 4 0例 ,均为行慢径消融术成功病例 ,对比消融前后和两组间的房室结功能参数 ,分析和比较这两组患者在射频消融前后房室结电生理特点的异同。结果　所有病例均消融成功。两组病例消融后较消融前房室结前传文氏周期及最长A2 H2 间期均缩短 ,而老年组的心动过速周长、消融前后窦性心率周长及消融后房室结前传文氏周期均较青年组延长。结论　老年人的房室结前传电生理特性较青年人为差 ,而对房室结折返性心动过速患者的慢径有效消融后 ,房室结电生理特性的变化规律不受年龄因素影响     

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。     

主动脉无冠窦内射频消融前间隔房室旁路

目的 报道经主动脉无冠窦内射频消融前间隔房室旁路.方法 7例患者,男性4例,女性3例,平均年龄（38.4±14.7）岁.电生理检查证实存在房室旁路,并检查其前传逆传功能和诱发旁路参与的房室折返性心动过速.在心动过速时标测最早心房逆传激动点作为消融靶点.结果 7例心动过速时最早心房激动部位均位于前间隔区域,但经右心房途径反复消融均不能成功阻断旁路,而在无冠窦内可标测到最早逆传心房激动点并消融成功,无并发症出现.结论 主动脉无冠窦内消融可作为治疗前间隔房室旁路的一种新途径,特别适用于右心房前间隔区域消融失败的病例.     

Impulse Formation and Conduction of Excitation in the Atrioventricular Node

AV Nodal Conduction. Meijler et al. have recently challenged the classical concept of AV nodal conduction (the conduction hypothesis) and suggest that the AV node might he controlling ventricular rhythmicity through its automaticity electrotonically modulated In atrial excitation (the modulated pacemaker hypothesis). This article critically evaluates the three major arguments of Meijler: (1) the absence of convincing evidence for conduction of excitation in the AV node; (2) the prevalence of disproportionately short AV intervals in larger animals; and (3) elimination of KR intervals shorter than the cycle length of ventricular pacing during atrial fibrillation, to judge which of these two hypotheses would more satisfactorily explain various experimental and clinical findings accumulated in the past. Previous observations including microelectrode mapping of the rabbit AV junction during regular sinus rhythm as well as second–degree AV block, clinical and experimental studies on concealed conduction, and studies on the ventricular response to atrial fibrillation appear to he compatible with the conduction hypothesis, whereas clearcut evidence for automatic impulse formation in the AV node has not been presented, except in a small number of hearts showing spontaneous AV junctional rhythms. In view of these observations and theoretical considerations based on comparative anatomy of the AV node–His–Purkinje system and on the latest experimental study on the equine AV node, the authors conclude that the conduction hypothesis appears to better explain all the available data, except perhaps in a few cases with second–degree intra–AV nodal block.     

Delineation of AV Conduction Pathways by Selective Surgical Transection: Effects on Antegrade and Retrograde Transmission

Introduction: The role for transitional cells as determinants of AH and HA conduction was examined in the superfused rabbit AV junction.Methods: Bipolar electrodes and microelectrodes were used to record antegrade A-H and retrograde H-A activation, before and after transection of the transitional cell input to the compact AV node.Results: During pacing from the high right atrium, inferior to the coronary sinus os, beneath the fossa ovalis, or on the anterior limbus, AV Wenckebach block (WB) was mediated by identical transitional cells grouped in close apposition to the compact AV node. Paced WB cycle lengths were shorter from the high right atrium (196 ± 12 msec) and inferior to the coronary sinus os (195 ± 8 msec) versus the fossa ovalis (217 ± 9 msec) or anterior limbus (206 ± 11 msec). With His bundle pacing, retrograde HA WB (211 ± 17 msec) was observed within the N cell region within the compact AV node. After transection of posterior and superior transitional cell input to the compact AV node, the antegrade AH WB cycle length was prolonged (245 ± 18 msec), with an increased WB incidence within the NH region (compact AV node)(5% to 41%; p = 0.014). The incidence of retrograde HA WB determined within the NH region was increased (30% to 88%), with a decrease in the stimulus-fast pathway conduction time (98 ± 7 to 49 ± 6 msec; p < 0.01).Conclusions: The data demonstrate (1) a common transitional cell population determining AH WB, independent of atrial stimulation site, and (2) a plasticity of transitional cell-compact AV node connections, with rapid AH and HA conduction favored by removal of posterior/superior AV nodal input.Supported by a grant from the American Heart Association, Oklahoma Affiliate.     

Role of the autonomic nervous system in the genesis of first and second degree atrio-ventricular nodal block

Thirty-four patients with a prolonged A-H interval (group I)and 26 with A-V nodal Wenckebach block (group II) were studiedin the basal state and after autonomic blockade (propranolol0.2mg kg^–1 and atropine 0.04 mg kg^–1 in order toassess the role of autonomic system in A-V nodal conductiondisturbances. In group I, the A-H intervals did not change significantlyafter autonomic blockade, whereas pacing cycle length for Wenckebachblock, effective and functional refractory periods of the A-Vnode decreased significantly (P<005). In the 22 patientswith organic heart disease these variables did not change significantlyafter autonomic blockade, whereas in the 12 without underlyingheart disease, they decreased in all cases (P< 0001). Inthe former, the variables of intrinsic A-V nodal conductionwere normal in only 6% of patients, whereas in the latter theywere normal in 66%. Also in group II, the intrinsic A-H intervalswere normal in only 6% of patients with cardiac disease butwere normal in 63% without underlying heart disease. These datasuggest that in the patients with first and second degree A-Vnodal block and organic heart disease, the conduction disturbanceis predominantly related to intrinsic involvement of A-V node,whereas in the subjects without underlying heart disease theA-V nodal blocks appear mainly related to autonomic alterations.     

A new terminology for describing left and right ventricular conduction abnormalities

The words we use to describe a medical condition should match our knowledge of it. Unfortunately, at times, the words we used long ago persist after new knowledge of the subject has become apparent; so it is with left and right ventricular conduction system abnormalities. The words left or right bundle-branch block no longer reflect our knowledge of the condition. Accordingly, this essay describes a new terminology that more accurately describes the numerous abnormalities that compose left and right ventricular conduction system block as well as their numerous subsets. A brief account of the cardiac conditions associated with the conduction defects is also presented.     

显性旁道射频导管消融术中顺传与逆传分离现象及原因分析

目的探讨显性旁道射频导管消融（下称消融）中顺传与逆传分离现象及其原因。方法对14例预激综合征患者行常规心内电生理检查及消融。结果右侧旁道12例,左侧旁道2例,初次有效靶点消融时均出现旁道顺传与逆传分离现象。2例左侧旁道证实为斜行旁道,后在逆传A波最早点继续消融成功,4例患者置入Swartz鞘管后在原理想靶点继续放电后成功消融,6例患者同样在原理想靶点基础上靠近心房侧或心室侧消融成功,2例患者为右侧双旁道,按常规方法标测消融另一隐匿性旁道。结论显性旁道消融中出现顺传与逆传分离现象,可能机制为旁道损伤、斜行旁道、宽旁道或多旁道。     

Decremental Conduction in the Posterior and Anterior AV Nodal Inputs

The role for fiber orientation as a determinant of conduction and block in the posterior (slow pathway, SP) and anterior (fast pathway, FP) AV nodal inputs was examined using multiple extracellular bipolar and intracellular microelectrode recordings in the superfused canine AV junction (N = 14). Results: In both inputs, antegrade longitudinal conduction velocity decremented in association with decreased action potential amplitude and dV/dt _max. A similar decrement was also present in the SP transverse to fiber orientation. SP conduction block occurred preferentially near its insertion into the compact AV node with very slow conduction (0.05 ± 0.01 M/sec) preceding conduction block. Distal antegrade FP conduction block occurred before conduction block occurred at more proximal FP sites. Conduction in the distal FP was maintained at a higher velocity (0.11 ± 0.01 M/sec, p < 0.05 vs. SP) before 2:1 conduction block was observed. Conduction velocity, action potential amplitude, and dV/dt _max were not different at any SP or FP site for paired activation transverse and longitudinal to fiber orientation. Conclusions: The data do not demonstrate a role for fiber orientation determining decremental conduction and block in transitional cell AV nodal inputs. Decremental conduction in both the SP and FP inputs is consistent with a proximal-to-distal gradient in resting membrane potential, action potential amplitude, dV/dt _max, and intracellular excitability in transitional cells during antegrade activation.     

阵发性心房颤动患者心房内阻滞的评价

目的对阵发性心房颤动(房颤)患者心房内阻滞的情况进行评价.方法入选78例阵发性房颤患者和8创无阵发性房颤的射频消融患者,电生理检查时分别放置高位右心房、希氏束、冠状静脉窦电极导管作起搏和标测用,在高位右心房进行S1S2程序刺激,S1刺激固定于500ms,S2从450ms开始,-10ms扫描,记录不同刺激时心房内和心房间传导时间及心房不应期.结果S1刺激时阵发性房颤组和对照组S1-AHB间期分别为(56.7±15.4)ms和(60.8±14.2)ms;S1-ACSd间期在两组分别为(110.2±24.3)ms和(107.5±25.6)ms;差异均无显著性(P＞0.05).S2刺激时,心房内传导时间最长延长1倍以上的患者在两组分别为15/78例和11/80例,心房间传导最长延长1倍以上的患者在两组间分别为13/78例和9/80例,两组间差异无显著性(P＞0.05).心房不应期在两组分别为(218.0±28.2)ms和(216.0±24.7)ms,两者间差异无显著性(P＞0.05).结论多数阵发性房颤患者无明显的心房内阻滞和不应期改变,传导时间延长也并非特异地发生在阵发性房颤组,提示心房内阻滞和不应期缩短在阵发性房颤的发生中的作用尚不明确.     

Bundle branch block on alternate beats during atrial fibrillation

This article reports a case of tachycardia-dependent right bundle branch block (RBBB) occurring during atrial fibrillation. In some sections of the recording, an alternans occurs between complexes with a complete RBBB pattern and complexes showing normal intraventricular conduction or incomplete RBBB. Alternans is frequently observed during phases of fast and nearly regular rhythm, but it occurs even in the presence of a markedly irregular ventricular response. The RBBB alternans associated with short and regular RR intervals is likely to represent a manifestation of 2:1 bundle branch supernormal conduction, whereas alternans occurring with irregular cycles expresses a complex interaction between the RR cycle length and some mechanisms affecting intraventricular conduction, such as tachycardia-dependent bundle branch block, supernormal conduction and concealed retrograde activation of the anterogradely blocked bundle branch (the so-called "linking" phenomenon).     

进行性心脏传导疾病

进行性心脏传导疾病以心内传导系统的进行性退行性变导致房室或室内传导阻滞,病因不明,体表心电图上出现PR间期及QRS间期的延长和/或左或右束支传导阻滞,病情严重时可导致晕厥或猝死.早期发病者预后差.患者常有钠通道基因异常的遗传性基础,诊断主要依赖心电图学的随访,因为发病率不明,临床应予以注意.治疗主要依赖永久性起搏治疗,适应证较其他传导系统疾病宽,抗心律失常药物治疗应谨慎.