单根电极VDD起搏器的初步应用（附七例报告）

自１９９４年１～１０月共为７例（完全性房室传导阻滞６例、高度房室传导阻滞１例）病人应用了单电极ＶＤＤ起搏器。术后随诊３～１２（平均６．５±２．５）个月，动态心电图监测全部达到心房同步起搏的目的，其中１例有个别间断性Ｐ波感知差而自动转为ＶＶＩ起搏，但总的Ｐ波感知率在９８％以上。如植入病例经严格选择（窦房功能正常的房室传导阻滞），单电极ＶＤＤ起搏可代替双腔ＤＤＤ起搏。     

VDD起搏治疗幼儿完全性房室阻滞(附一例报告)

一例３．５岁的女性幼儿因室间隔缺损修补术致迟发性完全性房室阻滞（ＣＡＶＢ）而安置ＶＤＤ起搏器。经锁骨下静脉途径埋置单根心房感知、心室触发起搏电极，使之于右房内塑形并贴靠房壁；起搏器埋于同侧皮下胸大肌筋膜上囊袋内。术中测得起搏阈值０．１Ｖ、脉宽０．４ｍｓ、电极阻抗５２０Ω、Ａ波振幅１．５ｍＶ、Ｖ波振幅１０．６ｍＶ，Ａ波感知设定０．２５ｍＶ。术后房室同步起搏率１００％，临床症状改善。表明ＶＤＤ起搏器不仅埋置简便，而且具有房室同步、频率应答等生理性起搏特点，是治疗幼儿ＣＡＶＢ的理想起搏方式。     

病态窦房结综合征生理性起搏治疗

对１１例ＳＳＳ患者安置了生理性起搏器，其中７例应用彩色三维超声心动图比较了心房按需型起搏（ＡＡＩ）、房室顺序起搏（ＤＶＩ）与单心室按需起搏（ＶＶＩ）三种不同起搏方式的血液动力学改变。结果显示ＡＡＩ、ＤＶＩ起搏较ＶＶＩ起搏每搏量明显增加分别达３７％、２０％（Ｐ＜０．０１）。通过程控调测、胸壁抑制试验、ＤＣＧ等定期随访患者心律失常及房室传导阻滞变化情况，在平均２０多个月的随访中尚未发现新的快速房性心律失常和传导阻滞，原有的房性心律失常也得到较好控制。认为ＳＳＳ患者的生理性起搏与ＶｖＩ起搏比较可产生较好的血液动力学效果，新的快速性房性心律失常及房室传导阻滞的发生率较低，因此对有适应症的ＳＳＳ患者应尽量选用。     

AAI起搏的临床应用观察

目前 ,生理性起搏多为心房起搏 (主要是ＡＡＩ型 )和房室顺序型起搏 (主要是ＤＤＤ型 )两种方式。前者更为经济 ,植入简便。本文总结 38例ＡＡＩ模式起搏的临床资料 ,现报道如下。临床资料本组行ＡＡＩ模式起搏患者 38例 ,男 2 3例 ,女 15例 ,平均年龄 6 0 7± 8 6岁。所有患者均无房室传导阻滞 (ＡＶＢ)。临床诊断包括传导系统退行性变 17例 ,冠心病 14例 ,高血压病 7例。起搏指征 :病态窦房结综合征 (ＳＳＳ) 37例 ,其中 30例为单纯窦缓、窦性停搏或窦房阻滞 ,7例为慢 快综合征 ;另有 1例为平行收缩性室性心动过速。 38例患者中 ,31例术…     

生理性心脏起搏的临床应用及参数选择

1991～1994年,我院共安置生理性心脏起搏52例(男32例,女20例;年龄33～69岁)。其中双腔心脏起搏(DDD)36例,双腔频率应答起搏(DDDR)2例,心房起搏(AAI)13例,心房频率应答起搏(AAIR)1例。诊断为病窦综合征30例、心肌炎Ⅲ°房室传导阻滞15例、双结病变4例、冠心病合并Ⅱ°Ⅱ型房室传导阻滞2例、风湿性心脏病合并三束支阻滞1例。术前对30例病窦综合征作经食管心房调搏检查,文氏阻滞点>120次/min者14例安装了AAI起搏器,文氏阻滞点<120次/min者安装了     

单根电极心室起搏双腔感知双重反应型起搏器心房感知功能的测试观察

目的：观察单根电极心室起搏双腔感知双重反应型起搏器（ＶＤＤ）心房电极感知功能的稳定性。方法：测试了１４例安装单根电极ＶＤＤ的患者在不同体位、扩胸运动及日常活动时的心房漂浮电极的最低感知阈值。并将术中测得的Ｐ波与术后测得的心房最低感知阈值做相关及线性回归分析。结果：１４例中有１２例患者不同体位的心房感知阈值不一致。其中９例在坐、立位时感知阈值最低，将心房感知阈值调至较最低感知阈值低两档的位置后做Ｈｏｌｔｅｒ检查，全部患者心房感知、房室顺序起搏功能良好。扩胸运动中无一例患者出现过度感知。术中所测Ｐ波振幅与术后测得的最低心房感知阈值相关性良好（ｒ＝０．６９，Ｐ＜０．０５）。结论：单根电极ＶＤＤ可替代双电极导管的双腔起搏双腔感知双重反应型起搏器（ＤＤＤ），用于窦房结功能正常的高度房室传导阻滞患者的起搏治疗。     

心房起搏脉冲传导延迟患者AV问期的优化

目的探讨心房起搏至心房除极波时间延迟患者设置起搏的房室间期（PAV）的方法及远期心房起搏的有效性。方法分析2005年1月至2012年12月我院起搏器植入后发生心房起搏至心房除极波时间延迟≥lOOms的患者10例,病窦综合征（SSS）患者的房室间期设置为最大值,并最大限度开启房室问期滞后功能;对房室传导阻滞（AVB）患者设置PAV的值为：140～180ms＋心房起搏至心房除极波延迟时间,不开启AV滞后。结果经1个月至7年随访,5例SSS患者心室起搏比例〈10％,3例SSS患者心室起搏比例30％。50％,Holter显示心室起搏时为假性融合波,l例SSS患者及1例AVB患者为心室起搏心律,起搏比例〉99％,保证了房室问期的生理性。10例患者心房起搏阈值均〈1．5／0．4ms,未发生心房起搏阈值增高及失夺获。结论心房起搏至心房除极波时间延迟患者远期的心房起搏夺获是安全的;设置起搏器PAV间期要将心房起搏至心房除极波延迟时间计算其中,程控随访中应注意观察程控仪中监护图的心房波,房室传导阻滞患者可延长房室间期后观察心房波,部分患者因监护导联显示不清,需要通过12导联心电图进行观察,避免心房起搏至心房除极波延迟病例被遗漏．导致增加心室起搏及非生理性的房室间期。     

儿童矫正性大动脉转位伴Ⅲ度房室阻滞的VDD生理性起搏(附一例报告)

一例１１岁矫正性大动脉转位（ＳＬＬ）的女性患儿有晕厥史１０年，超声心动图证实心内无分流，动态心电图及电生理检查均证实为Ⅲ度房室阻滞，窦房结功能正常。安置ＶＤＤ生理性起搏器，感知与起搏电极间距为１３ｃｍ，Ｐ波振幅２．２ｍＶ、心房感知０．７５ｍＶ、心室起搏阈值０．４Ｖ。术后观察心房感知率９８％。给心内无分流的心脏畸形患儿安置起搏器要充分考虑生理和生长发育的需要，如合理选择起搏器类型和电极长度，进行电生理检查测定心尖至高位右房的距离，同时熟悉复杂心脏畸形影像学的知识对保证安置术的成功十分必要。     

心房感知不良导致心室安全起搏1例

患者男性 ,６２岁 ,因病态窦房结综合征置入Ｂｉｏｔｒｏｎｉｋ公司产ＡｃｔｒｏｓＤＤＤＤ型起搏器 ,起搏参数为 :ＤＤＤ模式 ,基础频率６０次／ｍｉｎ ,滞后频率ＯＦＦ ,睡眠频率５５次／ｍｉｎ,上限频率１３０次／ｍｉｎ ,动态房室间期１８０／１００ｍｓ,安全房室间期 (ＳＡＶＤ)１００ｍｓ,心房、心室不应期为４２５／３００ｍｓ,心房、心室起搏电压均为３．６Ｖ ,起搏脉宽均为０．４ｍｓ,感知灵敏度为１．５／２．５ｍＶ ,心室空白期为２４ｍｓ。术后心电图示起搏器心房电极感知不良 ,心室频繁安全起搏。心电图 (图１)Ａ、Ｂ行心房感…     

心室停搏大于三秒的临床意义及起搏器应用的商榷

目的探讨心室停搏大于３秒作为安置起搏器的指征是否合适。方法收集动态心电图（ＤＣＧ）检查中具有３秒以上ＲＲ间期的７９例病例，分析心室停搏的发生原因及起搏器应用情况对生存率的影响。结果６１８０例次Ｈｏｌｔｅｒ记录中心室停搏大于３秒７９例（８６例次１．４％）。心室停搏发生于心房纤颤（房颤）心房扑动（房扑）中２７例（３４．２％），房室传导阻滞３例（３．８％），房颤、房扑终止后１９例（２４．０％），室上性心动过速终止后９例（１１．４％），窦性停搏及Ⅱ度窦房传导阻滞２１例（２６．６％）。起搏组及非起搏组各死亡３例，两组３年生存率无差异。结论安置起搏器要结合心室停搏的原因及相关症状而定，对发生在房颤、房扑中的长时间心室停搏一般不必安置起搏器，对无症状的病窦综合征患者推迟安置起搏器是安全的     

Familial occurrence of sinus bradycardia, short PR interval, intraventricular conduction defects, recurrent supraventricular tachycardia, and cardiomegaly.

Four members of a family presenting with sinus bradycardia, a short P-R interval, intraventricular conduction defects, recurrent supraventricular tachycardia (SVT), syncope, and cardiomegaly had His bundle studies and were found to have markedly shortened A-H intervals (30 to 55 msec.) with normal H-V times (35 to 50 msec.). Right atrial pacing at rates as high as 170 to 215 per minute failed to increase the A-H or H-V intervals significantly. The data are compatible with the presence of an A-V nodal bypass tract (James bundle) or even complete absence of an A-V node. Ventricular pacing and spontaneous ventricular premature beats resulted in a short ventriculoatrial conduction time (110 msec.) suggesting that if A-V nodal bypass tracts exist, they are utilized in an antegrade and retrograde fashion. None of the features of WPW syndrome was present. The mechanism of syncope in the mother and daughter was intermittent third-degree heart block. Both went on to develop permanent complete heart block despite electrophysiologic studies demonstrating 1:1 A-V conduction at extremely rapid atrial pacing rates and both required implantation of permanent pacemakers. The mechanism of syncope in the two brothers was possibly marked sinus bradycardia, but transient complete heart block has not been ruled out. Permanent pacemaker therapy was recommended for both. The nature of the cardiomegaly, which was mild in three patients, is not known. Although not well documented, several maternal relatives have had enlarged hearts, SVT, complete heart block, and syncope.     

Pacemaker syndrome and retrograde ventriculoatrial conduction

19 cases of pacemaker syndrome were observed in 121 patients implanted with VVI pacemakers. The main manifestations of pacemaker syndrome were dizziness, lightheadedness, fatigue, hypotension and congestive cardiac failure after permanent ventricular pacing. The incidence of pacemaker syndrome was 20% in patients with sick sinus syndrome and 13.2% with A-V block. Pacemaker ECG showed retrograde ventriculoatrial conduction in 25 of 121 cases. Among these patients, 14 (56%) had pacemaker syndrome, while only 5 of 96 cases without ventriculoatrial conduction had this syndrome, so the incidence of the two groups were quite different, P less than 0.0001. The frequency of ventriculoatrial conduction in patients with sick sinus syndrome was higher than in patients with A-V block (16/45 vs 9/76, P less than 0.05). The electrophysiologic study were performed in 17 cases before PM implantation. 3 cases had 170-190 ms ventriculoatrial 1:1 conduction. Retrograde ventriculoatrial conduction in pacemaker ECG were present during ventricular pacing in all of them.     

Tachycardia-bradycardia syndrome (so-called "sick sinus syndrome"). Pathology, mechanisms and treatment

The tachycardia-bradycardia syndrome consists of paroxysmal atrial fibrillation, flutter or tachycardia followed by sinoatrial block or sinus arrest resulting in Stokes-Adams attacks. Detailed histologie findings of the conduction system of 2 patients with this entity correlated well with the clinical observation of cardiac rhythm disturbances in the sinus node, atria and atrioventricular (A-V) junction. Eight other patients with the syndrome were studied clinically. The mechanisms (as revealed by the electrocardiogram) producing the bradycardia phase include depression of pacemaker function (arrest) or of conduction (exit block) of the sinus impulse, or both, plus depression of A-V junctional impulse formation. Proper therapy usually requires electrical pacing in conjunction with administration of digitalis or propranolol, or both. Our findings suggest that the term “sick sinus syndrome” is an inaccurate and inappropriate synonym for the tachycardia-bradycardia syndrome.     

Our experience using continuous atrial stimulation in sick sinus syndrome

Temporary atrial pacing (AAI) was applied in 31 patients with sick sinus syndrome (S.S.S.), including 20 with tachycardia-bradycardia syndrome (t.b.s.). In all patients before pacemaker implantation atrioventricular conduction was estimated using rapid left atrial, transoseophegeal stimulation assuming Wenckebach's point over 120 imp./min to be a physiological one. In all cases, but one ventricular electrodes were implanted and connected with multiprogrammable pacemakers (MP). Follow-up time ranged from 3 to 38 months (mean 18,4). Electrode dislodgment was not observed. In 9 persons sensing disorders were observed but thanks to programming the pacemaker sensitivity they could be resolved almost in all of them. Second degree Mobitz type I a-v block occurred in 3 patients during a long-term follow-up. In one of them changing the pacing mode to VVI was necessary. In persons with tachycardia-bradycardia syndrome cardiac pacing together with pharmacologic therapy allowed to almost eliminate tachycardia attacks. Authors positively estimated AAI pacing mode.     

AAI pacing mode: When is it indicated and how should it be achieved?

AAI pacing offers better hemodynamic characterstics than dual-chamber pacing and is the optimal mode for patents with sick sinus syndrome without AV conduction disorders. AAI pacing may be achieved by single-chamber atrial, by programming a dual-chamber pacemaker to the AAI mode, or by programming a dual-chamber pacemaker to DDD mode with a long AV delay. The annual incidence of AV block development in patients with sick sinus syndrome is low, probably 1-5%, but there is no method of detecting patients immune to future development of AV block. Chronotropic is often present in patients with sick sinus but the value of additional rate response is not yet established. Our recommendations for the choice of the method of pacing are discussed.     

Benefits and limits of single chamber atrial pacing with adaptive rate

Twelve patients with isolated symptomatic sinus node dysfunction or bradycardia-tachycardia syndrome with atrial chronotropic incompetence during exercise testing were managed by single chamber rate responsive atrial pacing (AAIR) when AV conduction was normal, or by a dual chamber DDDR pacemaker programmed in the AAIR mode when AV conduction was abnormal, and followed up for 12.5 +/- 9.8 months. The patients were assessed clinically, by 3 monthly ECG and Holter recordings and comparative exercise tests in AAI and AAIR modes at the 6th month. One patient with an AAIR system was excluded at M21 because of symptomatic AV block requiring reimplantation of a DDD pacemaker. Ten of the 11 remaining patients are asymptomatic and have an excellent quality of life; one patient had invalidating symptoms on exercise attributed to the "AAIR pacemaker syndrome" which were corrected by reprogramming the pacemaker and modifying the medical therapy. The comparative exercise stress tests showed a significantly higher heart rate in the AAIR mode compared to AAI pacing at the initial and intermediate exercise levels (30 to 70 W); on the other hand, the heart rates were not significantly different at the highest exercise levels although in the AAI mode, the terminal acceleration sometimes occurred in junctional rhythm whereas it was usually an atrial paced rhythm in the AAIR mode. The total duration of exercise was longer in the AAIR mode (+22%; p less than 0.01) when the 8/11 patients with chronotropic incompetence during the baseline study were considered. The spike-R interval adapted normally to exercise in only one case: in the other patients, the interval remained constant or, in the worst of cases (N = 4), it increased paradoxically, to result in the "AAIR pacemaker syndrome": this phenomenon is observed mainly in patients treated by antiarrhythmics and/or betablockers. The AAIR mode would therefore seem to be a simple, effective and reliable method of treating patients with sinus node dysfunction and chronotropic incompetence; however, the failure of adaptation of the PR interval is a real limitation to its use and may constitute an argument in favour of the choice of a DDR pacemaker in these patients.     

Intrahisian block in cardiomyopathy

Two patients with cardiomyopathy and intrahisian atrioventricular [A-V] block are described. The first patient with underlying non-obstructive hypertrophic cardiomyopathy had split His bundle potentials only during atrial pacing and presented associated conduction abnormalities: enhanced A-V nodal conduction and sick sinus syndrome. The second patient had progressive muscular dystrophy and a complete intrahisian A-V block. Attention is called to the possible interrelationship between different conduction abnormalities and to their clinical implications.     

Development of sinus node disease in patients with AV block: implications for single lead VDD pacing

OBJECTIVE: To investigate the incidence of sinus node disease after pacemaker implantation for exclusive atrioventricular (AV) block. DESIGN: 441 patients were followed after VDD (n = 219) or DDD pacemaker (n = 222) implantation for AV block over a mean period of 37 months. Sinus node disease and atrial arrhythmias had been excluded by Holter monitoring and treadmill exercise preoperatively in 286 patients (group A). In 155 patients with complete AV block, a sinus rate above 70 beats/min was required for inclusion in the study (group B). Holter monitoring and treadmill exercise were performed two weeks, three months, and every six months after implantation. Sinus bradycardia below 40 beats/min, sinoatrial block, sinus arrest, or subnormal increase of heart rate during treadmill exercise were defined as sinus node dysfunction. RESULTS: Cumulative incidence of sinus node disease was 0.65% per year without differences between groups. Clinical indicators of sinus node dysfunction were sinus bradycardia below 40 beats/min in six patients (1.4%), intermittent sinoatrial block in two (0.5%), and chronotropic incompetence in five patients (1.1%). Only one of these patients (0.2%) was symptomatic. Cumulative incidence of atrial fibrillation was 2.0% per year, independent of the method used for the assessment of sinus node function and of the implanted device. CONCLUSIONS: In patients undergoing pacemaker implantation for isolated AV block, sinus node syndrome rarely occurs during follow up. Thus single lead VDD pacing can safely be performed in these patients.     

病态窦房结综合征患者房室传导功能分析

为了解病态窦房结综合征患者的房室传导功能,用食管电生理检查观察窦房结功能正常者86例、窦房结功能低下者40例和病态窦房结综合征者109例的房室传导功能.结果显示:3组的文氏型阻滞点、2:1阻滞点差异无显著意义(P>0.05).将窦房结功能障碍者的窦房结恢复时间与文氏型阻滞点、2:1阻滞点作相关分析,结果均无相关性(P>0.05).认为病态窦房结综合征发生房室传导阻滞的概率较低,植入起搏器前应作食管心房调搏检查房室传导系统功能.     

The effect of atropine on cardiac arrhythmias and conduction. Part 2

The effects of atropine on various components of the specialized conduction system of the heart and the myocardium itself are reviewed. These actions are sometimes unpredictable or paradoxical, depending on the component showing the dominant effect and the health of the entire system. Atropine is best known for its chronotropic effect. Improved sinoatrial conduction has been demonstrated but the effect on the refractoriness of atrial muscle is unsettled. Atropine stimulates the atrioventricular (A-V) junctional pacemaker and facilitates conduction through the A-V node. The response of the subjunctional portion of the specialized conduction system to the drug is unpredictable and controversial in some respects.Atropine is useful in the diagnosis of sinus node dysfunction, in the evaluation of coronary artery disease during atrial pacing, and in attempting to produce normal conduction in patients with the Wolff-Parkinson-White Syndrome. Its principal therapeutic application is in correcting the hypotension-bradycardia syndrome occurring during acute myocardial infarction. It also has a role in the temporary management of sinus node dysfunction. Atropine may also cause arrhythmias, including atrial fibrillation, A-V dissociation, ventricular tachycardia, and ventricular fibrillation. The clinical settings in which atropine may be arrhythmogenic are discussed.