Kappa 700型双腔起搏器的临床随访

观察具有自动夺获功能的双腔起搏器 (Kappa 70 0 )置入后参数的变化和安全性情况。随访 1 3例置入Kappa70 0型起搏器患者 ,观察术中、术后 1周及术后 1 ,3,6个月心室起搏阈值、输出电压、输出脉宽、电极阻抗、R波振幅的变化 ,了解起搏器的工作情况。术后测得的起搏阈值较术中明显升高 ( 0 .71± 0 .2 3Vvs 0 .39± 0 .0 6V ,P <0 .0 5 ) ,术后不同时间测得的起搏阈值无明显差异。R波振幅术中、术后无明显差异。术后阻抗较术中明显降低 ( 62 5 .7± 1 2 3.0Ωvs 894.3± 1 90 .3Ω ,P <0 .0 5 ) ,术后 1个月后的阻抗基本稳定。起搏器自动夺获功能打开后 ,平均输出电压为 0 .96～ 1 .1 6V ,平均输出脉宽 0 .32～ 0 .34ms,平均心房感知灵敏度 0 .71～ 0 .83mV ,心室感知灵敏度 3.82～3.91mV。随访期间起搏、感知功能正常 ,无误感知现象。具有自动夺获功能的双腔起搏器输出电压低 ,安全可靠。     

起搏器自动夺获功能失活的观察分析

观察分析自动夺获(AC)功能无法正常工作的原因。41例患者置入具有AC功能的起搏器,术后1周、1个月、3个月随访体表心电图、动态心电图,应用程控仪进行遥测和程控,测定刺激除极波(ER)振幅、极化电位(PS)等参数,观察AC功能的工作情况。结果:41例经术后随访起搏器功能正常。5例(12.2%)在术中虽经多次调整电极位置,也无法术中使用AC功能。4例ER值始终低,极化电位较高(ER/PS<1.5);1例因噪声干扰太大,术中无法测试ER振幅。5例术中未能打开AC功能者,其中4例于1个月后随访时,ER/PS≥2,将AC功能打开。1例术中起搏电极位置在右室基底部者,R波感知>10mV,ER始终小于2.4mV,多次随访均无法安全使用AC功能。术中打开AC功能的36例中,术后随访时5例需关闭AC功能,其原因:①起搏阈值超高≥4.5V(1例),②大量室性融合波导致频繁后备脉冲释放(2例),③后备脉冲(4.5V/0.5ms)工作时的不适感觉(1例,伴室性融合波导致频繁后备脉冲释放),④局部肌肉抽动引起噪声干扰无法进行ER振幅测试(2例)。结论:多种因素都能影响起搏器AC功能。为保障起搏器可靠安全,低耗能状态,近期的随访观察尤为重要。     

具有自动夺获功能心室起搏器的临床观察

我科1998年1月至10月共植入具有自动夺获功能心室起搏器6例,男4例、女2例,年龄64.3±10.5岁。植入起搏器的适应证为病窦综合征2例、度房室阻滞2例、度型房室阻滞2例。其中合并阵发性心房扑动1例、合并阵发性心房颤动2例。植入起搏器均为Pacesetter公司的RegencySC (VVI型),电极亦为该公司提供的带有激素释放功能的低极化1470T双极电极。起搏器植入手术与普通VVI起搏器相同。术中除常规测定起搏阈值、阻抗、R波振幅外,尚需加测刺激除极波(ER)的振幅。术后当天,用APSu3250型程控仪将起搏器自动夺获功能打开。术后1周及1,3,6,9个月进行…     

具有自动夺获功能的心室起搏器临床应用

目的：评定15例心室起搏器的自动夺获功能的功效和安全性。方法：15例患者．男性9例，女性6例，年龄37～81岁，均有器质性心脏病．基础心律：10例为慢性心房颤动伴RR长间歇，4例病态窦房结综台征，其中2例合并阵发性心房颤动，1例三度房室阻滞。11例植人Regency SC＋型VVI起搏器，4例植人Regency SR-型VVIR起搏器。结果：起搏器植人后随访1～13个月，起搏器工作良好，QRS(R)振幅9．65±2．55mV．ER振幅785±3．87mV，两者相关系数(r）为0．15（h=55)。应用VARIO方法和自动夺获法测定的起搏阈值均在0．3～15V之间，两者相关系数为0．99(n=46)。极化电位低于lmV者占全部测定例次的e4G，高于1mV的极化电位幅度为1．38 0．13mV(n=37)。结论：与普通VVI(R)起搏器相比，具有自动夺获功能的VVI(R)起搏器功耗低，预计使用寿命长，起搏安全可靠，随访省时。     

连续夺获阈值监测与自动调节起搏器刺激输出——MICRONYSR＋起搏器多中心研究

目的：本研究评价具有心室自动夺获功能的Microny起搏器的安全性及功效。方法：自1994年11月至1996年9月欧洲国家的16个医学中心，共有113例植入Microny起搏器的患者进入了研究。所有植A的起搏器采用了Pacesetter的低极化、双极电极导线(Membrane 1402T)。患者在出院时及出院后1，3、6、12个月分别进行随访：结果：在植入后1个月的随访中一动态心电图显示所有未夺获的心搏均有后备起搏脉冲(4．5V／0．49ms)出现．植^时测试自身R波高度为14．7±7．4mV，刺激除极渡高度(ER)为10．2±4．8mV。这些数值随时间推移保持稳定，但二者无相关性(r=0.29)，植入时,由VARIO功能测试的起搏阈值为0．5±0.2V,由自动夺获功能测试的阚值为0．6±0．3V。两种方法测试的起搏阈值在各次髓访中相关性较好(r=0．79),平均差异为0.11V。后备起搏脉冲占起搏刺激的1．1％。发放后备起搏脉冲的原因为未能夺获(7．1％)；(伪)融合波(87．0％)；ER感知低下(0.5％)和QRS感知低下(4．1%)。在自动夺获功能打开时，起搏电流总消耗为1．4A。结论：本研究证明了自动夺获功能根据当时的起搏阈值安全和可靠地调节起搏器的输出一为患者提供最大的安全性并延长起搏器的使用寿命。     

具有自动夺获功能起搏器的临床应用

目的为评价具有自动夺获功能起搏器临床应用的初步结果。方法９例患者安装了具有自动夺获功能的起搏器（ＲｅｇｅｎｃｙＳＣ＋２４０２Ｌ），观察术后早期（术后１～２天）、术后１周、２周及术后远期（１～４个月）的起搏阈值、输出电压、ＥＲ振幅、阻抗及极化电位等参数变化。结果８例均能以自动夺获方式工作，输出电压随起搏阈值变化而变化。１例因自身心律与起搏心律形成融合波而致感知不足，导致“起搏阈值波动”。１例因极化电位升高而致自动夺获功能无法工作。结论具有自动夺获功能起搏器的临床应用表明其具有安全、省电的特点。     

有自动夺获功能的双腔起搏器的临床随访

目的观察双腔心室自动阈值夺获起搏器长期的参数变化及安全性.方法我院1999年10月至2000年6月住院植入具有心室自动阈值夺获功能的双腔起搏器20例,观察术中、术后1周、2周、1个月、3个月及6个月后的心室起搏阈值、输出电压、ER振幅、阻抗、极化电位及自动工作方式转换功能.结果术后早期心室起搏阈值、极化电位轻度升高,2周后趋于稳定,其余参数无明显变化,长期的心室起搏电压平均为(1.26±0.38)V.15例术后即刻可以启动自动夺获功能,4例术后1周可启动自动夺获功能,随访期间功能正常,无起搏脱漏现象,且5例伴有阵发性心房颤动的患者,心房颤动时均可发生工作方式转换,未出现起搏器介入性心动过速.1例肥厚梗阻性心肌病患者因术中及术后极化电位较高致自动夺获功能不能启动.结论有自动夺获功能的双腔起搏系统耗能低,安全可靠,满足了患者的生理需要.但对有心内膜病变患者有待进一步观察.     

房室顺序起搏系统A波振幅测量值的观察研究

观察术后平静呼吸时体位变化对房室顺序起搏系统A波振幅测量值的影响 ,并与术中测量值进行比较。安装DDD或VDD起搏器的患者 2 8例 (DDD 17例、VDD 11例 ) ,自主窦性心率大于 30次 /分 ,均无心房颤动或房性早搏。术后 7天采用起搏器程控仪BiotronikSWM 10 0 0的自动P/R波感知测试功能 ,分别测试患者平静呼吸状态下坐、卧位 12s的A波振幅 ,并与术中测量值进行比较。结果 :平静呼吸状态下DDD和VDD组的A波振幅测量值变化均较大 ;VDD型起搏器A波振幅测量值在坐、卧位有显著性差异 (P =0 .0 2 )。结论 :房室顺序起搏系统A波振幅测量值是一个易受呼吸、体位、术后时间等因素影响的参数 ,临床设定起搏器感知灵敏度时应动态了解A波振幅大小 ,及时调整感知参数 ,以保证有效安全的房室顺序起搏     

有自动阈值夺获功能的双腔起搏器的临床应用

目的:评价有自动阂值夺获功能的DDD起搏器的节能效果及起搏的安全性。方法:35例病人,其中男21例,女14例,植入有自动阈值夺获功能DDD起搏器后1周、2周、3周、1个月、2个月、6个月、1年、2年分别检测心室起搏阈值、输出电压及心室刺激除极波振幅和极化电位。结果:心室起搏阈值在术后2周达到最大值,由原来的0.42±0.32V升至1.05±0.82V,以后逐渐下降稳定于0.80±0.58V。心室自动阈值夺获功能打开后,心室起搏输出电压稳定于1.31±0.46V,明显低于普通起搏器的输出电压(2.5-4.5V),大大节省了能量输出。同时该起搏器由于具有电压4.5V,脉宽0.49ms的保护性起搏,保证了起搏的安全性。结论:有自动阈值夺获功能的DDD起搏器能自动调整起搏电压,高能量保护性起搏,节能效果好,而且安全。     

四岁儿童植入有自动夺获功能的起搏器一例

临床资料　患儿女性,4岁,因病毒性心肌炎,三度房室阻滞,心率40次/min和晕厥发作于1997年12月24日植入美国Pacesetter公司的2400LVVIR具自动阈值夺获功能起搏器,术中测试阈值电压0.6V,阻抗940Ω,R波振幅9.2mV,斜率1.79V/s。起搏器程控参数:频率70～130次/min,脉宽0.37ms,R波感知灵敏度3.0mV,不应期300ms。起搏器植入后每8h自动测试起搏阈值,并自动以高出起搏阈值0.3V进行起搏。术后1周程控显示起搏频率70～130次/min,阈值0.6～1.2V,输出电压0.9～1.5V,大大节省了输出能量。随访1年,起搏器阈值结果,其感知性能　　作者单位:200052　上海…     

具有自动夺获功能起搏器刺激除极波振幅的影响因素及远期随访

观察刺激除极波 (evokeresponse,ER)振幅及极化电位在远期随访中的稳定性及不同体位对其的影响 ,分析ER振幅与起搏器一般工作参数的关系。对 1996年 12月～ 1998年 12月之间收治的 2 4例埋置了RegencySC +2 40 2L永久起搏器的患者进行 2 .43± 0 .6 2 (2～ 3.5 )年的随访观察。结果 :ER振幅及极化电位在随访期间是稳定的 ,平卧位时ER振幅最低为 8.5 0± 3.0 2mV ,立位时最高达 9.32± 2 .95mV ,两者有统计学差异 ,P <0 .0 5。其他体位之间无差异。极化电位与体位变化无关。 2 / 2 4例分别因极化电位升高、ER振幅降低同时伴极化电位升高 ,而至自动夺获功能不能工作。ER振幅与起搏器一般工作参数无相关性。结论 :ER及极化电位在随访期间是稳定的 ,体位对ER振幅有一定影响 ,个别病例出现ER及 /或极化电位的变化 ,随访时应注意检测     

Long-term results of endocardial pacing with Autocapture threshold tracking pacemakers in children.

AIM: We aimed to evaluate the long-term results of endocardial pacing with Autocapture threshold tracking pacemakers in children. METHODS AND RESULTS: Implantation and follow-up data of 20 children with these pacemakers were retrospectively evaluated. The pacemakers were implanted subpectorally in five and subcutaneously in 15 patients. The indication for pacing was high-grade atrioventricular block in 18 cases. The mean age at implantation was 7+/-4.8 years. Four patients were pacemaker dependant (heart rate < 30 bpm). At implantation, the mean pacing threshold was 0.5 V at 0.5 ms. The mean evoked response (ER) signal was 8.5+/-3.6 mV, and the polarisation signal (PS) was <1 mV in 15 patients and 1-2 mV in five patients. During the mean follow-up period of 60 months, mean ER signal decreased significantly to 7.7+/-6.3 mV at 24 months and 6.5+/-2.5 mV at 60 months (P < 0.05). In four of 15 patients (26.6%), with a predischarge PS value of <1 mV, it increased between 1 and 2 mV over time. During follow-up, autocapture function was deactivated in six (30%) patients; due to inappropriate ER/PS values in four and due to severe muscle twitching in two with subpectoral implants. These problems occurred during a median period of 21 months after implantation. Generators were replaced in three patients with Microny pacemakers because of battery depletion at 54, 66 and 78 months. In two of them autocapture function had been working since implantation. In seven of 10 patients, who completed > or = 60 months of follow-up, battery impedances were still at the predischarge level. CONCLUSIONS: Autocapture function works well in most children at implantation. Mean ER signal significantly decreases over time despite stable pacing parameters. Autocapture function may become nonoperational due to decreased ER signal in some patients. Muscle twitching may be an important problem that may result in discontinuation of autocapture function in children with subpectoral implants.     

Long-term follow-up of pacemakers with an Autocapture pacing system

The aim of this study was to evaluate the safety and performance of the Autocapture pacing system during a 5-year follow-up period. The study was conducted retrospectively between May 1996 and May 2001. Sixty consecutive patients who had undergone VVI pacemaker implantation using an Autocapture program with leads 1402T (n: 31) and 1452T (n: 29) were included in the study. Intraoperative measurements including a ventricular stimulation threshold test, sensing of intrinsic R wave (mV), and lead impedance (W) were done by a standard pacing system analyzer. Evoked responses (ER, mV) and polarization signals (PS, mV) were measured after the pocket was closed. Pacing thresholds by Autocapture (AC thrd, V) and Vario (Vario thrd, V), battery current (mA), and battery impedance (kW) were also repeated during predischarge and 1, 6, 12, 18, 24, 30, 40, 50, and 60 months after discharge. According to the ER and PS values an Autocapture algorithm could be activated in 49 patients (88%). The Autocapture algorithm remained active during the follow-up in all of these patients. In patients with inappropriate ER and PS values (11 patients, 12%), pacemakers were programmed to a VVIR pacing mode and Autocapture algorithm was inactivated. ER and PS values did not reach appropriate values to activate the Autocapture algorithm in any of these patients in consecutive follow-ups. Twenty-four-hour Holter monitoring could be conducted in 32 patients (53%). In all recordings, when the loss of capture occurred, it was confirmed that back-up pacing continued. When the first measurements recorded during implantation were compared to approximately the 5th year measurements; ER (9.2 mV vs 9.6 mV), PS signal (1.13 +/- 0.30 mV vs 1.15 +/- 0.72 mV), AC thrd (0.4 V vs 1.2 V), Vario thrd (0.7 V vs 1.3 V), and lead impedance (502 ohm vs 620 ohm) were not changed significantly. Battery impedance increased 1 kOhm between 30-40 months of the implantation. Seven deaths occurred during follow-up. Three patients had fatal myocardial infarction, one died due to a non-cardiac event, and the remaining three died due to progressive heart failure. Conclusion: ER, R wave amplitude, and PS, which are the main parameters for the continuation of Autocapture function, did not change significantly during long-term follow-up. High output back up pacing provided additional safety for sudden rises in threshold. The Autocapture pacing algorithm was found to be effective and reliable during long-term follow-up.     

Pacing threshold changes after transvenous catheter countershock

The serial changes in pacing threshold and R-wave amplitude were examined after insertion of a countershock catheter in 12 patients referred for management of recurrent ventricular tachyarrhythmias. In 6 patients, values before and immediately after catheter countershock were monitored. Pacing threshold increased (from 1.4 ± 0.2 to 2.4 ± 0.5 V, mean ± standard error of the mean, p < 0.05) while the R-wave amplitude decreased (bipolar R wave from 5.9 ± 1.1 to 3.4 ± 0.7 mV, p < 0.01; unipolar R wave recorded from the distal ventricular electrode from 8.9 ± 1.8 to 4.6 ± 1.2 mV, p < 0.01; and proximal ventricular electrode from 7.7 ± 1.5 to 5.0 ± 1.0 mV, p < 0.01). A return to control values occurred within 10 minutes. In all patients, pacing threshold increased by 154 ± 30% (p < 0.001) during the first 7 days that the catheter was in place. It is concluded that catheter countershock causes an acute increase in pacing threshold and decrease in R-wave amplitude. A catheter used for countershock may not be acceptable as a backup pacing catheter.     

Acute effects of a class IA antiarrhythmic drug on the ventricular evoked response amplitude in patients with cardiac pacemakers

Some newer cardiac pacemakers are able to control the efficacy of the ventricular pacing pulse beat by beat and to adjust the ventricular output to the actual pacing threshold. This capture verification is based on the detection of the ventricular evoked response amplitude, which has to be detected immediately after the pacing pulse. The sensitivity of the pacemaker to detect the evoked response amplitude must be adjusted individually to avoid the simultaneous detection of lead polarization. The aim of the present study was to evaluate the acute effects of a class IA antiarrhythmic drug on the evoked response amplitude and polarization in 13 pacemaker patients. The implanted pacemaker was the VVIR pacemaker Regency (St. Jude Medical), which provides the automatic capture verification algorithm Autocapture. The patients received 50 mg of ajmaline intravenously within 1 min. The evoked response amplitude and polarization were measured before and 2, 4, 6 and 8 min after ajmaline injection. The evoked response amplitude significantly decreased from 8.0 +/- 4.0 mV to a minimum value of 6.4 +/- 3.1 mV 2 min after drug administration. The decrease remained significant from the end of the application up to 6 min. The recommended sensitivity setting for the evoked response significantly (p < 0.05) decreased from 4.0 +/- 2.3 mV before to 3.1 +/- 1.3 mV 2 min after administration. No significant changes were observed for polarization. After the ajmaline application in 2 patients, the pacemaker recommended the deactivation of Autocapture for 9 min in 1 patient and 12 min in the other. The reasons were a decrease in the evoked response amplitude from 3.1 to 1.9 mV and from 9.0 to 5.7 mV, respectively, with a polarization ranging to about 3.0 mV. In conclusion, the ajmaline injection decreased the evoked response amplitude for some minutes. These findings indicate that antiarrhythmic drugs can alter the automatic capture verification function.     

Correlation between changes in R wave amplitude and left ventricular volume induced by rapid atrial pacing

To examine the Brody effect in humans, we studied 15 patients by means of coronary sinus pacing. We measured left ventricular (LV) volumes from the cardiac output (measured by the thermodilution technique) and LV ejection fraction (measured by radionuclide ventriculography). Pulmonary blood volume was determined by means of cardiac output and mean pulmonary transit time. In six patients, pacing was performed at two different rates, resulting in 21 pacing measurements. The heart rate increased with pacing from 73 ± 11 to 119 ± 19 bpm (mean ± standard deviation, p < 0.001). The end-diastolic volume (EDV) and the end-systolic volume (ESV) decreased with pacing (p < 0.001 each). The R wave amplitude decreased with pacing (1.44 ± 0.63 mV control vs 1.32 ± 0.58 mV with pacing; p < 0.01). R wave amplitude decreased in 19 of the 21 pacing studies (90%); EDV and ESV decreased in all 21 pacing studies, and pulmonary blood volume decreased in 14 of the 15 pacing studies (93%) performed in 11 patients. There was a significant correlation between the percentage of change in R wave amplitude with the percentage of change in EDV (r = 0.54, p < 0.01) and with the percentage of change in ESV (r = 0.54, p < 0.01). These results, therefore, validate Brody's hypothesis and indicate that changes in LV volumes affect the R wave amplitude.     

主动固定电极在右心室不同部位起搏损伤电流变化

目的 探讨主动固定电极植入右心室心尖部及中位间隔部后损伤电流（current of injury,COI）的变化特点。 方法 入选88例右心室植入主动固定电极患者,分为右心室心尖组及中位间隔组。测定电极螺旋旋出0、5、10 min的COI及常规起搏参数,分析COI变化特点及相关关系。 结果 88例患者中有2例因心腔内电图（intracardiac electrogram,ICEG）振幅过大,其产生的COI无法准确测量。剩余86例患者测定的COI在主动固定电极螺旋旋出后逐步降低,5 min测定COI与0 min相比下降〔（6.6±1.5） mV vs.（7.6±1.7） mV,P<0.05〕,10 min测定COI与5 min相比显著下降〔（5.5±1.5） mV vs.（6.6±1.5） mV,P<0.05〕;螺旋旋出10 min后较0 min显著降低（P<0.01）。右心室主动固定电极测定的COI在心尖组及中位间隔组的差异无统计学意义。Pearson相关分析发现,0 min测定COI与起搏阈值之间呈负相关,相关系数（r）=-0.497,P<0.01。术后2例患者电极脱位,其COI均<5.0 mV。 结论 右心室主动固定电极螺旋旋出后COI值逐步降低,心尖组与中位间隔组COI的差异无统计学意义。0 min测定COI与起搏阈值之间呈负相关。     

Safety of Remote Magnetic Navigation in Patients With Pacemakers and Implanted Cardioverter Defibrillators

Magnetic Navigation and Implanted Devices. Background: Remote magnetic catheter navigation (MNS) has been shown to be feasible and safe for radiofrequency catheter ablation of various cardiac arrhythmias. However, its safety in patients with implanted pacemakers or cardioverter–defibrillators has not yet been studied. Objectives: This retrospective case series study intends to assess the acute and short‐term safety of remote MNS in patients with implanted pacemakers or cardioverter–defibrillators. Methods: Between January 2008 and June 2009, a total of 31 patients with implanted pacemakers (n = 5) or cardioverter–defibrillators (n = 26) underwent 32 catheter ablation procedures using the remote MNS. Baseline pacing thresholds, sensed amplitudes, pacing and, if available, shock impedances as well as battery status were measured in all devices before, immediately after, and 1–3 months after catheter ablation. Results: After ablation, no statistically significant difference in atrial sensing (2.7 ± 1.5 mV vs 3.1 ± 1.9 mV, P = 0.18) and impedance (457 ± 104 Ω vs 449 ± 101 Ω, P = 0.37) were observed. After ablation, no statistically significant difference in right ventricular sensing (10.4 ± 3.8 mV vs 10.9 ± 4.9 mV, P = 0.43) and impedance (535 ± 118 Ω vs 534 ± 120 Ω, P = 0.913) were observed. No changes in pacing threshold could be observed in all but 2 patients with biventricular cardioverter–defibrillators who underwent ventricular tachycardia ablation in lateral wall of left ventricle near the implanted epicardial electrode. Conclusions: Ablation procedures using remote MNS can be performed safely in patients with implanted devices with no significant effects on device system integrity. Long endocardial ablation close to the insertion site of the implanted epicardial left ventricular leads can affect the pacing and/or sensing characteristics of these electrodes. (J Cardiovasc Electrophysiol, Vol. 21, pp. 1130‐1135)