永久性心脏起搏器植入术中发生心房纤颤时心房电极导线定位经验

目的:研究永久性心脏起搏器植入术中心房纤颤(房颤)发作时以右心房波振幅最大处为右心房电极导线固定位置的可行性。方法:22例房颤发作时植入右心房电极导线的患者术中,测试右心房波振幅,术后随访恢复窦性心律(窦律)时测试右心房波振幅、起搏阈值,2者进行对比分析。结果:房颤心律时,所测得的右心房振幅与转为窦律后所测得的右心房波振幅有较好相关性,2者差异无统计学意义[(2.4±1.0)mv比(2.7±1.2)mv,P>0.05]。房颤时术中右心房波振幅平均(2.4±1.0)mv(1.6～3.7mv)者,在房颤转为窦律后所测定的心房感知和起搏功能良好。结论:在房颤发作时,右心房波振幅作为永久心脏起搏器合适的感知及起搏参数,有一定的临床实用价值。     

起搏器植入术中测试右心房A波振幅的价值

目的探讨阵发性房颤患者在房颤发作时植入心房电极的价值。方法 96例患者分为两组,84例窦性心律组和12例阵发性房颤组。两组均于窦性心律时或术中房颤发作时测试其右心房A波振幅。房颤组随访术后恢复窦性心律时的右心房A波振幅,并对窦性心律时和房颤发作时的右心房A波振幅进行对比分析。结果窦性心律组术中的右心房A波振幅为(2.6~9.5)m V(3.52±1.44)m V。阵发性房颤组术中房颤时右心房A波振幅为(1.3~3.1)m V(2.78±0.49)m V,两者差异无统计学意义(p0.05)。阵发性房颤组术后转复窦性心律即刻、术后3个月、术后6个月、术后1年测得的心房A波振幅分别为(1.8~4.5)m V(3.08±0.59)m V、(2.8~4.6)m V(3.19±0.49)m V、(2.7~4.8)m V(3.16±0.55)m V、(2.6~5.2)m V(3.13±0.69)m V,它们和房颤发作时测得的心房A波振幅差异无统计学意义(p0.05)。术后窦性心律时心房感知功能及起搏功能均良好。结论阵发性房颤发作时植入右房电极是可行的,右房A波振幅可作为植入的感知参数。     

心房颤动发作时心房电极的置入

目的:探讨心脏起搏器置入术中心房颤动(房颤)发作时置入心房电极的方法和可靠性。方法:对24例具有心脏起搏器安置指征的慢快综合征患者房颤发作时置入心房电极的方法、术中术后心房电极的参数进行分析。结果:所有病例全部成功置入心房电极。4例阵发性心房扑动(房扑)患者经超速刺激转复2例;普罗帕酮转复8例阵发性房颤、房扑患者4例成功,胺碘酮转复14例阵发性房颤患者6例成功,总转复率45%。12例术后复律后程控测得P波振幅、心房电极阻抗、起搏阈值与12例术中复律患者测得的参数差异无统计学意义(P>0.05);10例房颤患者术中测得心房波为(0.8±0.6)mV,明显小于术后复律后程控测得的P波(1.4±0.5)mV(P<0.05),但两者阻抗无明显差别(P>0.05)。结论:心脏起搏器置入术中房颤发作时置入心房电极安全可靠。     

VDD起搏器远期心房感知功能的观察

评价VDD起搏器远期心房感知功能的可靠性。 1 4例VDD起搏器病人 ,术后一周内每天记录心电图 ,术后32 .50± 1 3 .2 0个月时行Holter检查 ,检测过程中 ,让病人保持各种不同体位、做Valsalva动作、深呼吸、咳嗽及运动各2min ,并记录相应时间 ,手工检测 2 4h心房感知率。结果 :术后一周内 1 2例心房电极感知功能正常 ,1例于术后第 3天发生心房颤动 (简称房颤 ) ,经服用胺碘酮后恢复窦性心律 ,心房部分感知不良。 1例术后心房电极即无感知功能。Holter随访中 ,1 3例心房感知率为 88.98%± 2 8.35 % ,1例术后心房感知正常的病人 ,随访时动态心电图示持续房颤。结论 :对于绝大多数窦房结功能正常 ,因房室阻滞安装起搏器的病人 ,VDD起搏器远期心房感知功能比较可靠     

低位房间隔起搏对病窦综合症伴发作性房颤患者的临床应用

目的:探索低位房间隔起搏导线定位方法,评价房间隔起搏对病窦综合征患者房颤的预防作用。方法:病窦综合征患者48例,以X线及心电图特征定位,主动固定心房电极于低位房间隔,观察起搏后P波时限的变化及房颤的发作频率。结果:所有患者经房间隔起搏后,P波时限均显著缩短,118.00±24.00ms比93.00±16.00ms,差异有统计学意义;原有心房内传导延缓者,起搏后阵发性房颤发作频率明显减少,而心房内传导正常者,房颤发作无明显减少。结论:采用主动固定电极导线在低位房间隔起搏是安全、可行的,它能明显缩短左、右心房激动时间,使心房的除极趋于同步化;对伴房间传导阻滞者,房间隔起搏能减少房颤发作。     

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。     

双腔起搏器间歇性心房感知不良1例

患者男性，23岁。因发热咳嗽、胸痛3天伴黑噱1次入院。体检：BP120／60mmHg，神志清。超声心动描记术检查示先天性动脉导管未闭，右心房、右心室扩大。心电图（图略）示窦性心律，QRS波群形态正常，高度房室传导阻滞，室性逸搏心律，QRS波群呈右束支传导阻滞型。行动脉导管封堵术后数天植入双腔起搏器（Briotm D-220，心房双极，心室单极）。术中测试起搏参数为心房、心室起搏电压分别为0．5、0．5V，心房、心室阻抗分别为650、500Ω；腔内P波电压3．9mV，R波电压6．0mV，低限频率60次／min，高限频率120次／min。植入3天后动态心电图检查（图1）示A中的前半部分为窦性心律，频率83次／min，窦性P波后紧跟心室起搏，QRS波群增宽，主波向下，T波与心室除极波相反，心室起搏率与心房率相同。中间箭头所示起搏器出现心房感知不良，连续出现3次与前部分不同的“起搏”图形伴“钉样”信号，心室起搏QRS波群主波向上，与前部分不同；B中前半部分和最后两个心搏出现类似A中的起搏心电图，QRS波群主波朝上，中间出现P—R间期0．28s的正常QRS波群。X线胸片显示电极未脱位。心电图诊断：窦性心律，起搏器间歇性心房感知不良，安全起搏和干扰抑制，室性逸搏节律。     

《思考心电图之132》答案

窦性P-P间期0.80~0.84s,频率71~75次/min, QRS波群呈典型完全性右束支传导阻滞图形（时间0.13s）,其前均有低小心室起搏脉冲出现,P-R（V）间期固定为0.16s,且不以P-P间期的长短而改变,呈现“窦性P波-心室起搏脉冲-完全性右束支传导阻滞型QRS波群”,强烈提示该起搏器为双腔起搏器（心室为双极起搏）,心房电极感知窦性P波后通过设置的P（A）-V间期触发心室发放脉冲,呈现VAT起搏模式。形成这种QRS波群有以下3种可能：（1）窦性心律、完全性右束支传导阻滞、伪室性融合波群：即该QRS波群由窦性P波顺传,存在完全性右束支传导阻滞,心室起搏脉冲与QRS波群无关,仅重叠在QRS波群起始部形成伪室性融合波群,此种可能性最大。（2）心室起搏脉冲引发心室起搏形成该QRS波群：一般情况下,双腔起搏器的心室电极大多植入在右心室的心尖部,引发心室除极所形成的起搏QRS忆波群呈类左束支传导阻滞图形;当其起搏电极穿过室间隔植入左心室心内膜或误入冠状静脉的侧静脉所引发心室除极时,可形成类右束支传导阻滞图形QRS波群,但V1绝不会出现典型的三相波（rsR忆型）,此种可能性极小。（3）窦性心律、完全性右束支传导阻滞、室性融合波群：即窦性激动与心室起搏激动共同除极心室形成真性室性融合波群,但以窦性激动控制心室为主;从P-R（V）间期固定,且不以P-P间期的长短而改变及QRS波群呈典型完全性右束支阻滞图形看,此种可能性较小。〈br〉 综上所述,本例心电图诊断为：（1）窦性心律;（2）完全性右束支传导阻滞;（3）双腔起搏器,以VAT模式工作,其心房感知功能正常,而心房和起搏功能及心室感知功能未能评价;（4）伪室性融合波群。     

心房颤动消融术后窦性停搏与病态窦房结综合征患者起搏器植入术后参数对比

目的 比较心房颤动（下称房颤）射频导管消融术（RFCA）后窦性停搏与病态窦房结综合征（SSS）患者起搏器植入术后的电极参数。方法 选择2012年3月至2021年7月在宁波市第一医院心律失常诊疗中心因房颤RFCA术后窦性停搏植入起搏器者（RFCA-SA组）32例和SSS行起搏器植入术的患者（SSS组）124例。比较两组患者术中、术后3个月和术后1年的心房和心室电极的感知和起搏阈值。结果 术中、术后3个月和1年,RFCA-SA组患者心房感知低于SSS组,心房起搏阈值高于SSS组,差异均有统计学意义（均P<0.01）,而两组患者心室感知和心室起搏阈值比较,差异均无统计学意义（均P>0.05）。结论 房颤RFCA术后窦性停搏患者起搏器植入术后心房感知和起搏参数劣于单纯SSS患者。     

经永存左上腔静脉植入起搏电极体会

目的总结经永存左上腔静脉（PLSVC）植入起搏电极体会。方法总结4例PLSVC植入双腔起搏器的患者。患者出院前及出院后3个月、6个月进行随访,了解起搏器工作状态。结果4例患者术前均常规行经胸超声心动图检查,结果显示冠状静脉窦开口扩大,提示PLSVC存在可能。第1例患者因术前发现PLSVC可能,首先穿刺右侧锁骨下静脉;造影显示右上腔静脉缺如,右侧锁骨下静脉汇入PLSVC。第2、3例患者因双腔起搏器植入前反复出现心动过缓相关症状,在术前经右侧锁骨下静脉植人临时起搏器,术中造影显示PLSVC与右侧上腔静脉无交通。第4例患者在置入导丝时直接经PLSVC进入右心房。患者术后3个月、6个月常规行起搏器程控并调整起搏器出厂设置参数,此后每6—12个月行起搏器程控,程控时测量心房电极和心室电极的起搏阈值、感知和阻抗。均在满意范围。第1例患者两次随访时心律均为窦性心律,心房电极感知大于2mV,起搏阈值小于1V,阻抗小于1000Q。结论PLSVC能够顺利完成起搏电极植入。     

Blind atrial pacing for patients with sinus node disease who develop atrial fibrillation during permanent pacemaker implantation

During a 6-year period, six of 110 patients implanted with AAI pacemakers for sick sinus syndrome developed atrial fibrillation at the time of pacemaker implantation (5.5%). In all cases a passive fixation lead was sited in the right atrial appendage, its stability being ensured by rotation of the lead and phrenic nerve stimulation excluded by pacing at 10 V. One patient remained in chronic atrial fibrillation. In the other five, who subsequently reverted to sinus rhythm, atrial P-wave sensing and lead threshold values were satisfactory, allowing programming of the pacemaker output down to 2.5 V to conserve the battery. One out of these five patients continued to have intermittent atrial fibrillation. We conclude that in sick sinus syndrome, atrial fibrillation complicates AAI pacemaker implantation procedure in 5.5% of cases. As an alternative to an unplanned general anaesthetic to cardiovert the patient, it is reasonable to implant an atrial lead in the right atrial appendage in the expectation of a spontaneous reversion to sinus rhythm with a good lead threshold and P-wave sensing. In contrast to inappropriate pacing of the right ventricle in VVI mode, this strategy avoids pacemaker syndrome and reduces the risk of subsequent attacks of atrial fibrillation.     

Bipolar atrial sensing thresholds in sinus rhythm and atrial tachyarrhythmias. A comparative analysis in patients with DDDR pacemakers.

Automatic mode switching (AMS) function in dual chamber pacemakers depends on adequate detection of atrial tachyarrhythmias. There are few data on showing how intra-operative atrial signal amplititude during sinus rhythm can predict atrial tachyarrhythmias after pacemaker implantation. In 43 patients undergoing DDDR pacemaker implantation and atrioventricular nodal ablation for the treatment of drug-refractory paroxysmal atrial fibrillation, atrial sensing thresholds during sinus rhythm and during induced atrial tachyarrhythmias (24-48 h after device implantation) were analysed. Five different DDDR pacemaker systems were implanted (Chorus 7034, Ela Medical n = 13; Meta DDDR 1254, Telectronics Pacing Systems n = 12; Vigor DR 1230, Guidant n = 6; Trilogy DR 2364, Pacesetter, n = 2; Kappa DR 401, Medtronic USA n = 10). Every patient received a steroid-eluting, screwing, bipolar atrial lead (Medtronic, Capsure-Fix 4068). The mean P wave amplitude during implantation was 3.91 +/- 1.14 mV. The mean atrial sensing threshold during sinus rhythm and during all modes of induced atrial tachyarrhythmias was 3.35 +/- 1.0 mV, and 1.52 +/- 0.92 mV, respectively (P < 0.001). Atrial fibrillation was induced in 36 patients. The mean sensing threshold during sinus rhythm in this patient group was 3.39 +/- 1.01 mV, the mean sensing threshold during atrial fibrillation was 1.27 +/- 0.56 mV, reflecting a 63% reduction of sensing threshold compared with sinus rhythm (P < 0.001). Atrial flutter was induced in seven patients. The mean sensing threshold during sinus rhythm was 2.92 +/- 1.19 mV, the mean sensing threshold during atrial flutter was 2.79 +/- 1.26 mV, reflecting a reduction of 5% (ns) compared with sinus rhythm. Atrial sensing thresholds during sinus rhythm were significantly correlated with sensing thresholds during atrial tachyarrhythmias (r = 0.44; P < 0.002), but there were significant variations in intra-individual results. The reduction of atrial sensing thresholds between sinus rhythm and induced atrial tachyarrhythmias ranged from 30% to 82%. CONCLUSION: Bipolar atrial sensing thresholds during sinus rhythm are correlated with sensing thresholds during atrial tachyarrhythmias, but there is a large degree of variance in individual patients. A 4:1 to 5:1 atrial sensing safety margin based on sensing threshold during sinus rhythm is a predictor for adequate postoperative detection of atrial tachyarrhythmias and the function of AMS devices.     

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。     

The effect of drugs and lead maturation on atrial electrograms during sinus rhythm and atrial fibrillation

Antitachycardia devices need more accurate means to identify arrhythmias. Previous studies have found that sinus rhythm can be distinguished from a variety of tachyarrhythmias by algorithms that are based on time-domain and frequency-domain analysis of intracardiac electrograms. Amplitude distribution analysis (time-domain) and power density spectral analysis (frequency-domain) are two of the techniques that have seemed to hold promise. However, previous studies have not evaluated whether lead maturation or drugs such as lidocaine, propranolol, verapamil, or isoproterenol can interfere with the ability of these algorithms to distinguish among cardiac rhythms. In the present study, five dogs had permanent atrial pacing leads placed. On a series of days, recordings were made from the atrial leads during sinus rhythm and induced sustained atrial fibrillation, both before and after administration of cardioactive drugs. For up to 1 month after implantation, progressive lead maturation did not prevent differentiation of atrial fibrillation from sinus rhythm by either amplitude distribution analysis or power density spectral analysis. However, the difference between the power density spectra of sinus rhythm and atrial fibrillation became progressively less with time. Isoproterenol, lidocaine, verapamil, and propranolol had no consistent effects on amplitude distribution analysis of atrial electrograms during sinus rhythm or atrial fibrillation. However, there were marked effects of drugs on amplitude distribution characteristics in individual dogs. Propranolol and lidocaine produced consistent changes in power density spectra during sinus rhythm and atrial fibrillation, respectively; both drugs reduced the ability of power density spectral analysis to differentiate sinus rhythm from atrial fibrillation.(ABSTRACT TRUNCATED AT 250 WORDS)     

最小化心室起搏减少病态窦房结综合征患者心房颤动的发生

目的 探讨最小化心室起搏对病态窦房结综合征(病窦综合征)患者心房颤动(房颤)发生的影响.方法 入选2003年4月至2008年4月因病窦综合征植入DDD起搏器的患者112例,随机、单盲分为最小化心室起搏组56例(A组),和传统双心腔起搏组56例(B组),分别于3、6个月进行随访,以后每年1次,每次随访内容包括病史询问、起搏器程控、超声心动图.主要观察指标为房颤发生率,次要观察指标为超声心动图(包括左心房内径、左心室舒张末内径和左心室射血分数)和因心力衰竭再入院情况.结果 平均随访时间为(33.7±17.1)个月,与B组相比,A组的心室起搏平均比例显著减少(10.1%vs92.3%,P＜0.001),但两组的心房起搏平均比例相近(73.6%vs72.8%,P=0.98).B组累计房颤发生率明显低于A组(RR=0.65,95%可信区间0.59～0.93,P=0.015).与植入前相比,A组各阶段超声心动图变化差异无统计学意义;而B组左心房内径逐渐增大.术后2年起,B组左心房内径与植入前相比,或与同期的A组相比,差异有统计学意义.结论 右心室心尖部起搏使病窦综合征患者房颤发生率增加,左心房内径增大.因此,对房室传导正常的病窦综合征患者,建议最小化心室起搏,鼓励心室自身传导.     

Placement of atrial pacing leads during atrial fibrillation. Feasibility and subsequent lead performance.

AIMS: To assess the feasibility of placing permanent atrial pacing leads during atrial fibrillation (AF) and whether such leads function satisfactorily. METHODS AND RESULTS: Prospective study of 17 consecutive patients in whom permanent atrial leads were positioned during an episode of paroxysmal AF. Fluoroscopic position ('figure of 8' or side-to-side movement and anterior position in RAO projection), lead impedance (> 300 but < 1000 ohms) and intracardiac electrogram (average peak to peak amplitude > 1 mV) were used to define an acceptable lead position. At 8 weeks post implant we measured: pulse duration pacing threshold at 5 V; lead impedance at 5 V and 0.5 ms; intracardiac electrogram (EGM) signal amplitude. At the end of the study we reviewed patients to establish whether AF had become permanent. In all patients, follow-up demonstrated satisfactory lead function. All leads had impedances between 300 and 1000 ohms. Pacing thresholds were all < 0.1 ms at 5 V. Mean atrial EGM amplitude seen in sinus rhythm was 3.3 mV (range 1.2-8.4); in patients where all follow-up was in AF in was 2.1 mV (range 1.5-2.5). Nine patients (53%) developed permanent AF. CONCLUSION: Placing atrial leads during AF is feasible using the technique described. However, some patients progress to chronic AF, eliminating the benefits of atrial pacing.     

Atrial lead placement in the right atrial appendage during recent or chronic arrhythmia

An atrial arrhythmia could be encountered during the atrial lead implantation. The lead placement must subsequently be delayed after restitution of the sinus rhythm or completely abandoned. The authors investigate the atrial lead placement during atrial arrhythmia and the lead performance at 6-month follow-up. The study population was 65 patients aged 78.5 years, 42 males and 28 structural heart diseases. They were implanted for sick sinus syndrome (n=14), atrioventricular block (n=44), infra-hisian conduction abnormality (n=7) in association with an atrial fibrillation (63.1%), an atrial flutter (24.6%) or an atrial tachycardia (12.3%). The onset of the arrhythmia was < or = 7 days (47.7%) or > 7 days (52.3%). An atrial lead was placed in the right atrial appendage under fluoroscopic control. If the sinus rhythm was not restored at 1 month, an electrical cardioversion was performed. The per-implantation atrial signal amplitude was 2.2+/-1.5 mV (range 0.5 mV to 7 mV). Sinus rhythm was restored in 54 patients. At 1 month, one patient was in an incessant atrial fibrillation. The 53 patients in sinus rhythm had a good atrial lead performance. Out of 46 patients who completed the 6-month follow-up, 4 had an arrhythmia recurrence. The 42 patients in sinus rhythm had a good atrial lead performance. At 1 and 6-month follow-up, the atrial pacing threshold (1.1+/-0.7 V vs 1.2+/-1.0 V, ns) and the atrial signal amplitude (2.1+/-1.0 mV and 2.1+/-0.9 mV, ns) were stable. Comparing the patients with a recent or a chronic arrhythmia, the pacing thresholds (1.2+/-1.1 V vs 1.14+/-0.8 V, ns), the atrial signal amplitudes (2.17+/-0.9 mV vs 2.05+/-0.9 mV, ns) and the proportion of satisfactory pacemaker performance in DDD(R) mode for the patients in sinus rhythm (100% vs 100%, ns) did not statistically differ between the two groups at 6 months. In conclusion, the placement of an atrial lead in the right atrial appendage during an atrial arrhythmia is feasible with a good lead performance at 6 months in sinus rhythm regardless the onset time of the arrhythmia and provides a satisfactory atrial-based pacing with the preservation of the atrioventricular synchrony.     

Treatment of atrial fibrillation with an implantable atrial defibrillator--long term results.

OBJECTIVES: To evaluate the long-term outcome with an implantable atrial defibrillator (IAD) in patients with recurrent atrial fibrillation (AF). BACKGROUND: Maintenance of sinus rhythm using repeated internal cardioversion shocks has been shown to be effective and safe in short-term studies but long term follow-up is unknown. METHODS: Since 1995, 136 patients (30 women) with symptomatic, drug-refractory atrial fibrillation were implanted with an IAD (METRIX, InControl). This analysis was performed after a median of 40 (range 7-66) months after implantation. RESULTS: In 26 patients, the programmed mode was not documented during last follow-up, four patients had died. Of the remaining 106 patients (mean age 58+/-10, range 34 - 79 years), 39 were actively delivering therapy with the device, in 14 patients the device was used to monitor the arrhythmia but no shocks were delivered, and in 53 patients it was turned off or explanted. Increases in defibrillation thresholds (n=7), patient intolerance of multiple cardioversion shocks (n=15), and significant bradycardia requiring dual-chamber pacing (n=12) were the main reasons for discontinuation of therapy in addition to battery depletion (n=19). After explantation, efforts to maintain sinus rhythm were continued in 17 patients whereas rate control was attempted in 36 patients. CONCLUSIONS: A strategy of maintaining sinus rhythm long-term with an IAD is feasible in a proportion of patients. However, patient selection is critical, and technical improvements (i.e. higher shock energies, dual-chamber pacing and additional preventive and anti-tachycardia pacing algorithms) are required to increase the number of patients having long term benefit, and frequent arrhythmia recurrences and patient intolerance to repeated cardioversion shocks remain a major limitation.