不同部位起搏对阵发性心房颤动患者心房激动时间的影响

目的　比较右心耳 (RAA)、冠状窦远端 (DCS)、右心房双部位 (右心耳加冠状窦口 ,DSA)和双房 (右心耳加冠状窦远端 ,Bi A)起搏对阵发性心房颤动 (PAf)患者心房激动时间的影响。方法 2 2例接受心脏电生理评价试验的PAf患者在窦性心律下行心房不同部位起搏 ,同步记录 12导心电图 ,测量最大 P波时限。结果　与窦性 P波时限相比 ,RAA起搏明显延长 P波时限 (P<0 .0 1) ,DCS、DSA及 Bi A起搏则明显缩短 P波时限 (P<0 .0 1,P<0 .0 1,P<0 .0 1)。结论　 DCS、DSA及 Bi A起搏明显缩短心房激动时间 ,减少心房电活动的离散度 ,有利于 PAf的防治。     

心房起搏治疗心房颤动

近年来起搏器新功能如自动频率夺获心房起搏方式 ,频率平稳功能 ,频率适应性功能的出现 ,以及双心房同步或心房多部位起搏技术的临床应用 ,明显提高了心房起搏的抗心律失常作用 ,使心房起搏已成为治疗心房颤动 (房颤 )的重要、有效的方法。　　一、治疗和预防心房颤动的心房起搏方式　　按照心房起搏部位 ,治疗和预防房颤的心房起搏可分为两种 1单部位心房起搏 [1] :单部位心房起搏的位置可在右心耳、高位右房、右侧房间隔、界嵴、冠状静脉窦开口附近等部位。右心耳是目前最常采用的部位 ,仅需被动固定方式的心房导线电极则可。而高位右房或…     

心房起搏脉冲传导延迟一例

患者女性 ,40岁 ,因病窦综合征置入起搏器 ,配用IS 1BI双极心房 /心室电极 ,心房电极于右心耳起搏时参数较好 ,但电极难以固定 ,无SP间期 (起搏脉冲至P波的时限 )延长 ;于是行右房上部起搏 ,发生起搏脉冲传导延迟 (SP间期 14 0ms)。术后起搏器工作正常 ,SP间期为 10 0ms。产生其SP延迟的原因不太明确。     

冠状静脉窦口起搏对心房激动时间影响及方法学探讨

目的观察冠状静脉窦口起搏对心房激动时间的影响，并探讨该部位起搏的方法学。方法包括两部分，首先对20例射频消融的患者行心内电生理检查，术中分别给予高位右心房（HRA）、冠状静脉窦口（CS9-10）、左心房游离壁（CS1-2）起搏，记录刺激信号至腔内电图最远A波为心房激动时间；HRA至CS1-2的AA间期作为左、右心房间激动时间差，同时测量体表心电图最长P波时限。第二部分研究在可控弯导丝系统的辅助下将心房主动电极导线固定在冠状静脉窦口，比较冠状静脉窦口起搏与HRA起搏的起搏参数及起搏后体表心电图P波时限。结果冠状静脉窦口起搏时P波时限、心房激动时间及左、右心房激动时间差较窦性心律下、高位右心房及左心房游离壁起搏时均明显缩短。两组患者术中及术后起搏参数差异无统计学意义，冠状静脉窦口起搏患者体表心电图P波宽度明显缩短。结论冠状静脉窦口起搏时心房激动时间明显缩短，左、右心房间激动时间差最短。采用可控弯导丝系统的辅助可实现冠状静脉窦口起搏。     

不同部位心房起搏对心房电活动的影响

目的 观察右心耳及房间隔起搏对心房电活动的影响。方法 对DDD永久起搏器安置术109例（右心耳电极72例、房间隔电极37例）术前、术后分别描记体表12导联心电图，测量右心耳及房间隔起搏前后最长P波时间（Pmax）及P波离散度（Pd）。结果 右心耳起搏方式，Pmax及Pd较术前明显增加，而房间隔起搏方式Pmax及Pd较术前显著减少（P均〈0．05）。结论 房间隔起搏方式使心房电活动较稳定，有助于预防房性心律失常。     

快速心房激动对心房肌电生理特性的影响

比较快速心房起搏与急性心房颤动 (简称房颤 )诱发心房电生理特性的变化。以 15 0～ 2 0 0ms起搏周长(PCL)对 4 5例成功射频消融后 (RFCA)病人右房进行S1S1刺激诱发急性房颤 ,据能否诱发急性房颤分为非房颤组和急性房颤组 ;再以 4 0 0msPCL对心房快速激动前后高位右房、低位右房、His束周围等多部位进行S1S2 扫描 ,测定心房有效不应期 (ERP)、ERP离散度 (ERPd)、右房内及房间的传导时间的变化 ;另以 35 0 ,4 0 0和 4 5 0ms三个PCL随机对RAA进行S1S2 扫描 ,观察ERP频率自适应性的变化。两组心房快速激动后 4 0 0msPCL下右房各刺激部位及三种不同PCL右心耳ERP均较心房快速激动前有明显的缩短 ,并且缩短的程度相同。两组病人心房快速激动前后房内和房间传导时间及ERPd没有明显改变。两组心房快速激动前后斜率均值均较激动后明显下降 ;心房快速激动前、后斜率均值两组间无显明差别 (P >0 .0 5 )。结论 :两种方式的心房快速激动可诱发相似的心房电重构现象。     

射频消融治疗心房肌肌袖相关的房性心动过速

目的研究房性心动过速(房速)的临床和电生理特点.方法病例为1998年1月～2001年4月在我院因房速[部分伴心房颤动(房颤)]而行心内电生理和射频消融的患者.比较不同部位起源房速的临床特点和心内激动差异.结果共19例,年龄(46.8±18)岁.尝试消融治疗16例,房速起源右房侧11例,分别为希氏束上方4例,上腔静脉、右心耳各2例,下腔静脉、冠状窦口、终末嵴各1例.起源于左房侧5例,分别为肺静脉4例,左心耳1例.消融成功13例(81%),不成功者分别为希氏束旁2例,肺静脉1例.左房起源和上腔静脉起源房速心电图aVL导联P波呈负相,不同之处是后者Ⅰ导联P波呈正相.左上肺静脉、左心耳和上腔静脉起源的房性早搏(房早)和房速冠状窦远端心房激动早于或等于冠状窦口.而右上肺静脉房早和房速的冠状窦口激动早于远端.左上肺静脉、冠状窦口和下腔静脉的房早和房速时的冠状窦口激动早于右房上部.其他起源房早和房速时的右房上激动早于冠状窦口.成功消融部位电位提前体表心电图的P波(37.6±16.6)ms.但肺静脉和上腔静脉心动过速病例中各有1例经消融隔离心动过速起源的远端而成功.虽然多数患者的心动过速起源于易形成肌袖的心房和血管交界部位,但是肺静脉起源房速[AA间期(230.8±58.O)ms]的频率显著快于其他部位者[AA间期(342.6±86.5)ms,P=0.015],且更易出现房颤(4例全部出现).成功病例随访1～30(10±10)个月,无复发.结论局灶房速好发于心房与其他结构交界的部位,可能与该部位心房肌肌袖的存在有关,常规心内电生理检查有助于初步定位房速起源部位,射频消融成功率高.     

射频消融治疗起源于心房下部局灶房性心动过速

对6例起源于右房下部及3例起源于冠状静脉窦口局灶性房性心动过速(简称房速),行常规心内电生理检查,明确房速时心房激动顺序,寻找心房激动最早起源点标测与消融,临床随访评价疗效。结果:6例右房下部房速心电图Ⅱ、Ⅲ、aVF、V1导联P′为负,Ⅰ、aVL为正,3例冠状窦口部房速心电图Ⅱ、Ⅲ、aVF及V1导联P′波为负\正双向,Ⅰ、aVL P′低平,不易区别。成功消融靶点双极电图A-P间期40±15 m s。结论:体表心电图可大致区分房速起源部位。     

双心房一右室间隔上部三腔起搏

目的 探讨双心房一右室同隔上部三腔生理性永久心脏起搏的临床应用、心电生理学和血液动力学效应。方法为一缺血性心肌病并难治性心力衰竭患者植入冠状窦电极于心大静眯中段，“J”型电极于右心耳．专用主动螺旋电极于右室间隔上部．分别同步起搏左．右房和右室，组成新三腔起搏方式，应用swar-chnz导管和平衡法棱索心室造影测定不同起搏方式下心室／心房相位变化，心电生理学和血液动力学参数。结果双心房一右室间隔上部三腔生理性心脏起搏可产生较窄的QRS波和双房一致的撤动及正常的心室收缩顺序，并导致LVEF、RVEF和CO增加。结论 双心房一右室间隔上部三腔全生理性心脏起搏可能有益于某些伴有快速房性心律失常的心动过缓或心力衰竭患者的电生理学和血藏动力学改善。     

冠状窦导线与三腔起搏

目的 特殊设计的冠状静脉窭(冠状窦)导线用于三腔起搏，治疗病态窦房结综合征(病窦综合征)伴阵发性快速房性心律失常患者。方法三条电极导线(冠状窦、右房、右室)分别放置于冠状窦、右心房、右心室。双心房导线通过一个Y形接头和心室导线分别连接到DDD起搏器的心房和心室部分，行三腔起搏。结果4例(男3例，女1例)患者冠状窦导线均置于其中段．右房导线3例置于右心耳．1倒位于右房中外侧。右心室导线3例位于右室心尖部，1例位于右室中外侧。1例合并左上腔静脉畸形．右室导线通过冠状窦在右房绕一个圈进人右室心尖部。术中阈值测试．输出电压(V)、电流(MA)、阻抗(n)、PR波振幅(mV)分别为冠壮窦：0．56、0．76、744、4．4(P波)；右心房：0．56、1．2、467、6．3(P波)；右心室：0．6、0．9、613、17．6(R波)，脉宽固定于0．5ms。近期随访均呈DDD工作方式，起搏与感知功能良好，未发生房性快速心律失常，无并发症。结论特殊设计的冠状窦导线固定良好，三腔起搏性能可靠，方法可行，适用于房室阻滞或病窦综合征合并阵发性房性快速心律失常患者。     

Novel electrophysiologic parameter of dispersion of atrial repolarization: comparison of different atrial pacing methods

INTRODUCTION: Heterogeneity of ventricular repolarization plays a major role in reentrant tachyarrhythmias in cardiac tissue. However, the role of atrial repolarization added activation time (AT) to refractoriness in atrial vulnerability has not been investigated in detail. METHODS AND RESULTS: The study population consisted of 34 patients: 18 with atrial fibrillation (AF) and 16 without AF (control group). The effective refractory periods (ERPs) in the right atrial appendage, low lateral right atrium, high right septum, and distal coronary sinus, and ATs from P wave onset to each electrogram during sinus rhythm and right atrial appendage, low lateral right atrial, high right septal, distal coronary sinus, and biatrial pacing were measured. Atrial recovery time, defined as the sum of AT and ERP, and its dispersions during sinus rhythm, right atrial appendage, low lateral right atrial, high right septal, distal coronary sinus, and biatrial pacing were calculated. Both ERP dispersion and atrial recovery time dispersion during sinus rhythm were significantly greater in the AF group than in the control group. Atrial recovery time dispersion during distal coronary sinus, high right septal, or biatrial pacing was significantly smaller than that during right atrial appendage or low lateral right atrial pacing in each group. In particular, atrial recovery time dispersion during distal coronary sinus pacing was the smallest of the five pacing methods in the AF group. P wave duration during biatrial or high right septal pacing was significantly shorter than during right atrial appendage, low lateral right atrial, or distal coronary sinus pacing in each group. CONCLUSION: Atrial recovery time dispersion is suitable as an electrophysiologic parameter of atrial vulnerability. Distal coronary sinus pacing may prevent AF by increasing homogeneity of atrial repolarization, whereas biatrial and high right septal pacing contribute not only homogeneity of atrial repolarization but also improvement of atrial depolarization.     

Does A-H interval accurately represent intranodal conduction time during ectopic rhythms?

In order to determine whether the A-H interval of the His bundle electrogram accurately represents the AV nodal conduction time under various conditions, His bundle and coronary sinus electrograms were recorded in isolated perfused rabbit hearts, with atrial stimulation from eight different sites. The S-A (stimulus to the A wave) interval was significantly longer, whereas the A-H interval was shorter on stimulations from the coronary sinus and the left atrium than on sinus nodal stimulation. Stimulations from the fossa ovalis and right atrial appendage did not significantly alter the A-H interval. The effective and functional refractory periods of the AV node were almost identical with stimulations from the sinus node, low right atrial appendage, low left atrial appendage or the ostium of coronary sinus. Mapping of the excitation process with microelectrodes revealed that the activation times in low interatrial septal fibers bordering the His bundle [abbreviated as AP(III)] was closest to the A wave as compared with the activation in the ostium of the coronary sinus [AP(I)] or near the AN region [AP(II)] on stimulation from both sinus nodal and coronary sinus regions. On sinus nodal stimulation, AP(III) preceded AP(I) and AP(II) but lagged behind the A wave by 6 msec, whereas AP(III) preceded the A wave by 5 msec on coronary sinus stimulation. Thus, the A-H interval may not always accurately represent the intranodal conduction time, as relative timing of atrial activation responsible for the A wave and that of invasion of the AV node by the atrial wavefront can be grossly altered by different atrial excitation patterns.     

Effects of atrial pacing site on atrial and atrioventricular nodal function.

The effects of the site used for atrial pacing on atrial and atrioventricular nodal conduction were assesed in 16 patients. In 13 patients, three atrial pacing sites were used: high right atrium, low lateral right atrium, and midcoronary sinus. Two recording sites were used: low septal right atrium, including His electrogram, and high right atrium. Stimulus (S) to high right atrium interval was longest with coronary sinus pacing (76 plus or minus 7 ms) (P less than 0.001), and shortes with high right atrial pacing (41 plus or minus 3 ms) (P less than 0.05). There was no significant difference in stimulus to low septal right atrium from all three pacing sites. Atrial functional and effective refractory periods were not significantly different. Mean low septal right atrium to His was significantly shorter from the coronary sinus (93 plus or minus 8 ms) (P less than 0.001), as compared to high right atrium (139 plus or minus 16 ms), and low lateral right atrium (129 plus or minus 13 ms) pacing. AV nodal functional and effective refractory periods, and the paced rate producing AV nodal Wenckebach were not significantly different when comparing the three sites. Left atrial appendage and high right atrium were similarly compared in three additional patients, and no significant differences were found in conduction times and refractory periods.     

Effects of atrial pacing site on atrial and atrioventricular nodal function.

The effects of the site used for atrial pacing on atrial and atrioventricular nodal conduction were assesed in 16 patients. In 13 patients, three atrial pacing sites were used: high right atrium, low lateral right atrium, and midcoronary sinus. Two recording sites were used: low septal right atrium, including His electrogram, and high right atrium. Stimulus (S) to high right atrium interval was longest with coronary sinus pacing (76 plus or minus 7 ms) (P less than 0.001), and shortes with high right atrial pacing (41 plus or minus 3 ms) (P less than 0.05). There was no significant difference in stimulus to low septal right atrium from all three pacing sites. Atrial functional and effective refractory periods were not significantly different. Mean low septal right atrium to His was significantly shorter from the coronary sinus (93 plus or minus 8 ms) (P less than 0.001), as compared to high right atrium (139 plus or minus 16 ms), and low lateral right atrium (129 plus or minus 13 ms) pacing. AV nodal functional and effective refractory periods, and the paced rate producing AV nodal Wenckebach were not significantly different when comparing the three sites. Left atrial appendage and high right atrium were similarly compared in three additional patients, and no significant differences were found in conduction times and refractory periods.     

Author index: Volume 42

The various patterns resulting from stimulation through the catheter electrodes recording His bundle activity were evaluated in 30 patients using intracardiac electrograms from the right ventricular apex (RVA), posterosuperior wall of the left ventricle (LV), high right atrium (HRA) and left atrium (LA) in the vicinity of the coronary sinus. His bundle pacing was characterized by a QRS complex and stimulus (St)-V, St-RVA and St-LV intervals that equaled the QRS configuration, H-V, H-RVA and H-LV intervals of sinus beats. Right septal pacing produced a pattern of “complete” left bundle branch block (with normal electrical axis) associated with St-V intervals of 0 msec, and St-RVA and St-LV intervals of different duration from that of the H-RVA and H-LV intervals recorded during sinus rhythm. Fusion beats resulting from simultaneous activation of His bundle and right septal muscle were characterized by St-V Intervals of 0 msec and St-RVA or St-LV Intervals of similar duration to that of the H-RVA or H-LV intervals of sinus beats. Fusion QRS configuration depended on the type of ventricular complex present during sinus rhythm. Analysis of the retrograde atrial activation intervals permitted differentiation among impulse initiation at the low right atrium, His bundle or right septal muscle.Simultaneous recording of multiple atrial and ventricular electrograms has enhanced understanding of the complex patterns observed during attempted His bundle pacing in man.     

Ectopic right atrial rhythms: experimental and clinical data

In 18 out of 25 canine hearts studied with bipolar plunge electrodes, ectopic right atrial (RA) beats were observed occurring (1) spontaneously, (2) during vagal stimulation, (3) after destruction of the sinus node, and (4) during ventricular pacing. In these beats the RA appendage was activated first, followed by Bachmann's bundle, sinus node, left atrial appendage, posterior left atrium, and proximal coronary sinus. This sequence was consistently reproduced by pacing through the RA appendage recording electrode.     

Comparison of the acute effects of pacing the atrial septum, right atrial appendage, coronary sinus os, and the latter two sites simultaneously on the duration of atrial activation

OBJECTIVE—To compare the acute effects of right atrial appendage, atrial septal, coronary sinus os, and dual site pacing on the duration of atrial activation.
METHODS—20 patients with a variety of cardiac conditions underwent an intracardiac electrophysiological study. Electrograms were recorded from the right atrial appendage and at multiple sites within the coronary sinus. The duration of atrial activation was measured during pacing at the right atrial appendage, atrial septum, and coronary sinus os, and also during dual site stimulation.
RESULTS—The duration of atrial activation with atrial appendage pacing was notably longer (p < 0.001) than with dual site, septal, or coronary sinus os pacing, but there were no significant differences in atrial activation times between these latter three pacing modes. When stimulating the atria at a cycle length of 500 ms, the mean (SD) duration of atrial activation was 145 (37) ms for right atrial appendage pacing, 93 (26) ms for dual site pacing, 96 (28) ms for septal pacing, and 98 (28) ms for coronary sinus os pacing.
CONCLUSIONS—Assuming that the duration of atrial activation is an important determinant of predisposition to paroxysmal atrial fibrillation, atrial septal pacing or coronary sinus os pacing would appear to offer the same advantage as dual site pacing without the additional complexities associated with the latter pacing mode.


Keywords: atrial septal pacing; dual site pacing; atrial activation; atrial fibrillation     

主动脉无冠窦内和二尖瓣环-主动脉连接处射频导管消融局灶性房性心动过速

目的报道13例主动脉无冠窦内和1例二尖瓣环一主动脉连接（MAAJ）处成功消融局灶性房性心动过速（房速）,探讨该类房速的电生理特点及标测和消融方法。方法14例患者,男性3例女性11例,平均年龄（54．4±10．4）岁,均有阵发性房速病史。心房刺激诱发房速后,分析体表心电图P’波特点并于右心房进行激动标测,如果最早心房激动邻近希氏束附近,少数患者在此处消融,其他患者和上述消融不成功患者,经主动脉逆行途径,在无冠窦内标测和消融。如果消融不能成功,则经房间隔穿刺途径至左心房标测最早激动部位处消融。结果房速发作时体表心电图P’波明显变窄（77．8±14．4）ms。右心房激动标测均在希氏束附近标测到相对提前的心房激动,3例于此处消融失败。14例经主动脉逆行途径于无冠窦内标测到最早心房激动提前希氏柬处心房激动0～20．0（10．1±6．3）ms,13例于无冠窦内消融成功,包括1例改用盐水灌注导管后消融成功。1例经无冠窦消融失败后,经穿刺房间隔于MAAJ处标测到最早心房激动处消融成功。随访3～38个月,均无复发。结论对于具有窄P’波及标测右心房最早激动位于希氏束附近的局灶性房速,经主动脉逆行途径在无冠窦内标测和消融具有很高的成功率,经穿刺房间隔在左侧MAAJ处消融或应用盐水灌注导管无冠窦内消融可能进一步提高消融成功率。     

心房不同部位拖带法鉴别不典型房室结折返性心动过速和房性心动过速

目的报道一种鉴别不典型房室结折返性心动过速(AVNRT)和起源点邻近Kock三角的房性心动过速(AT)的新方法。方法 22例室上性心动过速患者,在心房不同部位(右房心耳部、冠状静脉窦近端、远端)起搏拖带心动过速,测定起搏后VA间期(最后一个起搏脉冲前传夺获的心室电图到起搏终止后第一心搏的最早心房电图的距离)。计算各部位起搏后VA间期的差别并取差别绝对数的最大值定义为ΔVA间期。结果 13例AVNRT起搏后ΔVA间期5.8±3.6(0～14)ms,9例AT起搏后ΔVA间期62.8±24.2(21～98)ms。ΔVA间期在所有AVNRT均<15 ms,在所有AT均>15 ms,因此起搏后ΔVA间期>15 ms用于诊断AT的灵敏度和特异度均为100%。结论心房不同部位起搏拖带法可用于准确鉴别不典型AVNRT和起源点邻近Kock三角的AT。