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。     

采用螺旋电极导线行右室流出道间隔部起搏的经验

目的介绍主动固定螺旋电极在右室流出道间隔部起搏中的应用经验。方法86例起搏适应证患者随机分成两组,一组42例采用主动固定螺旋电极行右室流出道室间隔起搏(简称主动电极组),另一组44例应用被动固定电极行右室心尖起搏(简称被动电极组),观察两组有关手术指标及主动电极组的起搏参数。结果主动电极组电极操作时间长于被动电极组(18.4±7.7 min vs 16.6±6.5 min,P<0.05),起搏QRS波时限则明显短于被动电极组(0.138±0.046 s vs 0.162±0.020 s,P<0.01);主动固定螺旋电极植入后起搏阈值达高峰,15 min后即降至稳定水平(0.78±0.26 Vvs 0.54±0.27 V,P<0.05);主动电极组1例发生电极脱位。结论主动固定螺旋电极在右室流出道室间隔起搏中是可行的、安全的,植入方法是关键。     

右室螺旋电极植入的参数变化

目的观察右室螺旋电极旋出后即时、20 min及术后1个月随访的电极参数变化,探讨右室螺旋电极的参数变化规律。方法回顾分析植入右室螺旋电极患者依术中腔内心电图及参数测试调整电极固定部位,分别固定于右室流出道、间隔部及心尖部;观察术后并发症及右室螺旋电极旋出后即时、20 min及术后1个月随访的电极参数变化。结果 1共入选57例均植入手术成功,其中电极固定于右室流出道26例,间隔部25例,心尖部6例,电极旋出后即时、20 min心尖部较间隔部及流出道起搏阈值明显增高(P均0.05);2电极旋出20 min后阈值下降30%左右;随后阈值又会缓慢渐渐升高,术后1个月接近于即时的阈值(P0.05),阈值变化在达到安全起搏范围内存在"两峰一谷"的曲线;3螺旋电极旋出固定后1个月较20 min后的阈值变化幅度和变化比例大(P0.05)。结论为保证术后长期的安全起搏,主动螺旋电极旋出前起搏参数满意而旋出后即时阈值增高时,也必须尽量追求电极旋出即时阈值达标。     

主动固定电极在右室流出道间隔部起搏中的应用研究

目的评价主动固定电极在右室流出道间隔部起搏应用中的可行性和稳定性。方法160例起搏适应证患者随机分为两组,每组80例,一组采用主动固定电极行右室流出道间隔部起搏(简称主动固定电极组),另一组应用被动固定电极行右室心尖起搏(简称被动固定电极组),观察电极置入时间和心电图QRS波宽度,电极置入后随访观察起搏阈值、感知、阻抗,电极脱位及相关并发症。结果主动固定电极组的置入时间和X线曝光时间均长于被动固定电极(26.34±6.54minvs20.86±4.32min,16.78±5.38minvs8.67±4.52min;P均<0.01)。主动固定电极组电极置入15min时较置入即刻的起搏阈值明显下降(0.76±0.21mVvs1.12±0.25mV,P<0.01)。主动固定电极组起搏的QRS波时限较被动固定电极组短(0.14±0.04msvs0.16±0.03ms,P<0.01)。术后随访1,3,6个月,两组的起搏阈值、感知、阻抗均无差异,未见电极脱位等并发症。结论主动固定电极在右室流出道间隔部起搏中的应用是可行和稳定的。     

采用主动固定电极导线行右室流出道间隔部起搏的临床应用

目的比较右室主动固定电极和被动电极导线应用结果,探索右室主动固定电极导线临床应用的可行性。方法需要安置心脏起搏器患者59例,其中男20例、女39例;年龄在75.6±23.8(54~92)岁。患者为缓慢性心律失常或者严重心力衰竭。30例被动电极组,固定部位为右室心尖部;主动电极组29例,电极固定部位为右室流出道。结果主动电极组与被动电极组即刻起搏参数比较没有明显的差异(起搏阈值:0.62±0.19V vs0.78±0.09V,P>0.05)。在出院后1,3,6个月随访起搏阈值与置入时比较也没有差异。只有1例出现主动电极从右室流出道间隔部脱位。主动电极置入时间和曝光时间较被动电极明显延长(45.03±1.99min vs13.69±11.37min;17.88±7.23min vs9.78±3.55min,P均<0.05)。结论使用主动固定电极进行右室流出道间隔部起搏是可行和安全的。     

静脉注射利多卡因对慢性期心室起搏阈值的影响

观察静脉注射 (静注 )利多卡因对慢性期心室起搏阈值的影响。对 12例起搏器安置术后 3个月以上的随访患者静注利多卡因 2mg/kg ,用相应的体外程控仪测试用药前、用药后即刻、15min、30min、2h的心室起搏阈值。结果 :8例患者出现起搏阈值升高 ,其中 2例起搏阈值超过 2 .5V ,出现起搏夺获缺失。用药后即刻平均起搏阈值由用药前的 0 .55± 0 .12V升至 0 .93± 0 .6 9V(P =0 .0 4 ) ;15min时升至 1.0 5± 0 .6 9V(P =0 .0 2 ) ;30min时则恢复至静注前水平。结论 :单剂量静注利多卡因 2mg/kg可使慢性期心室起搏阈值显著升高。     

静脉注射普罗帕酮对慢性期心室起搏阈值的影响

观察静脉注射 (简称静注 )单剂量普罗帕酮对慢性期心室起搏阈值的影响。安置起搏器 3个月后的患者 30例 ,随机单剂量静注普罗帕酮 70mg或 14 0mg,用相应的体外程控仪测试用药前后心室起搏阈值。结果 :固定脉冲宽度 (脉宽 )为 0 .5ms或 0 .4 9ms时 ,普罗帕酮 70mg组用药前、用药后即刻、30min、2h的起搏阈值分别为 0 .5 7± 0 .13,0 .5 1± 0 .12 ,0 .5 9± 0 .10 ,0 .5 4± 0 .11V ;14 0mg组分别为 0 .5 8± 0 .14 ,0 .5 4± 0 .13,0 .5 7± 0 .14 ,0 .5 2± 0 .12V。结论 :单剂量静注普罗帕酮对慢性期心室起搏阈值没有影响。     

右室流出道室间隔主动电极和右室心尖部被动电极的对照研究

目的探讨采用主动电极行右室流出道(RVOT)室间隔起搏的可行性和安全性。方法需要安置体内埋藏式心脏起搏器的100例患者,随机分为二组,50例用主动固定电极行RVOT室间隔起搏术(主动电极组),50例用被动固定电极行右室心尖部起搏术(被动电极组),记录两组在术中及术后的各项参数并进行比较。结果两组均顺利完成手术,未出现严重并发症。两组固定次数、曝光时间无差异(1.7±1.3次vs1.3±0.5次,7.9±5.2minvs5.4±4.4min,P均>0.05)。主动电极置入后即刻可达到理想阈值,比被动电极高(0.6±0.27Vvs0.5±0.25V,P<0.05),被动电极阻抗比主动电极高(911±225.31Ωvs668±168.03Ω,P<0.05),两组的感知阈值无差异。术后随访1个月时,两组的起搏阈值无差异。主动电极组2例,被动电极组1例出现导线脱位。结论使用主动电极行RVOT室间隔起搏是安全可行的。     

右心室间隔部起搏的安全性及可行性研究

目的 评估在接受心室起搏的患者中,应用右室间隔部起搏技术的安全性与可行性。方法:慢性心房颤动伴长RR间歇或缓慢心室率需植入水火起搏器患者10例,男性7例,女性3例,平均年龄64.20±12.61岁;心功能正常2例,NYHA Ⅰ级3例,Ⅱ级3例,Ⅳ级2例,因慢性心房颤动所有患者采用抑制型按需心室起搏模式(VVI)。术中首先将螺旋电极固定于右室心尖部(RVA),15分钟后测试起搏阈值;然后将螺旋电极移开右室心尖部,在X光影像学和心电图提示下,将螺旋电极最终固定于右室间隔部(RVS),15分钟后测试起搏阈值。结果 术中10例患者利用螺旋电极均成功进行了RVS的固定,未发生螺旋电极导线的移位、脱位或其它并发症。右室间隔部起搏阈值电压为0.73±0.36V,电流1.14±0.44mA,阻抗646.20±130.52Ω,R波振幅12.14±3.41mV。结论 对于慢性心房颤动伴长RH间歇或缓慢心室率患者,利用螺旋电极进行右室间隔部起搏可行且较为安全。     

心脏起搏器主动与被动固定电极置入后参数的变化

目的比较主动固定电极(螺旋电极)与被动固定电极术后各参数的变化。方法对18例接受被动固定电极及15例螺旋电极置入的患者,分别于术中;术后1,2周;1,2,3,6个月在平静状态下测定起搏阈值,A、V波振幅及阻抗。结果15例放置螺旋电极者,术后心房、心室阈值较术中下降(P<0.05);18例放置被动固定电极者,心房及心室电极术后起搏阈值无明显变化;全部33例术中;术后A、V波振幅测定值均无显著性差异(P>0.05);所有患者术后阻抗较术中明显降低(P>0.05),术后1周至6个月电极阻抗稳定,未出现显著性变化。结论安置螺旋电极者起搏阈值较术中下降,安置被动固定电极组起搏阈值无明显变化;而电极阻抗均较术中明显下降,长期随访稳定。     

固定螺旋主动固定导线植入早期及后期参数变化与安全性评价

目的 评价固定螺旋主动固定导线（Fineline Ⅱ EZ,美国波科公司）植入术中及术后3个月参数变化情况,评价其安全性.方法 2012年1月至2013年9月在青岛大学附属医院156例缓慢性心律失常患者行单腔或双腔起搏治疗,心室起搏导线均选用固定螺旋主动固定导线,经左或右侧锁骨下静脉置于右心室流出道间隔部,分别于导线旋入心肌即刻、旋入后5 min、术后即刻、术后3个月测试起搏参数：起搏阈值、导线阻抗和R波幅度,并观察术后有无导线脱位、导线穿孔、与经静脉有关的血栓形成及囊袋感染等严重并发症发生.结果 导线旋入即刻起搏阈值较高,5 min后明显下降[（0.76±0.22）V对（0.39±0.13）V,P＜0.001];术后即刻阈值较旋入5 min后进一步下降[（0.35±0.10）V对（0.39±0.13）V,P＜0.001].R波幅度在导线旋入后5 min测试较术后即刻降低[（12.70±4.94）mV对（8.94±4.07） mV,P＜0.001].术后仅1例患者出现导线脱位,无导线穿孔、囊袋感染等并发症发生.结论 固定螺旋主动固定导线旋入心肌5 min后起搏阈值明显降低,故可常规于旋入5min后进行测试,确定是否需要调整导线位置.固定螺旋主动固定导线在应用过程中是安全有效的.     

Acute changes in the pacing threshold after lead implantation. Comparison between retractable and sweet-tip active-fixation leads

Although the pacing threshold of steroid-eluting active-fixation leads remains stable over the long term, it changes rapidly after screw-in. We compared the pacing threshold in the acute phase between retractable and Sweet-Tip active-fixation leads. We studied 132 patients who were implanted with active-fixation leads for new pacemaker implantation or additional leads required due to disconnected/leaking leads. Pacing threshold was measured at 4 time points: before screw-in, immediately, and 5 and 10 minutes after screw-in. If the pacing threshold was > 1.5 volts (V) at 5 minutes, we changed the pacing site so that it became ≤ 1.5 V. A total of 169 retractable leads (Medtronic: 107 leads, St. Jude Medical: 62 leads) and 33 Sweet-Tip leads (Boston: 33 leads) were implanted. Eighty-nine leads were implanted in the atrium and 113 leads in the ventricle. Seventy patients were implanted with both atrial and ventricular leads. The pacing threshold of Sweet-Tip leads increased immediately after screw-in, while that of retractable leads decreased (Sweet-Tip: 0.20 ± 0.57 V, Retractable: -0.15 ± 0.53 V, P < 0.05). The pacing threshold of both types of leads decreased similarly from immediately to 5 minutes after screw-in (Sweet Tip: -0.29 ± 0.43 V, Retractable: -0.25 ± 0.36 V, P = NS). Few changes in the threshold were detected between 5 and 10 minutes. Because the pacing threshold of Sweet-Tip active-fixation leads increased immediately after screw-in and that of both type leads decreased from immediately to 5 minutes, we should measure the pacing threshold from 5 minutes after screw-in.     

主动固定电极导线行心脏特殊部位起搏的临床应用

目的探索主动固定电极导线行心脏特殊部位起搏临床应用的可行性和安全性。方法需要安置心脏起搏器患者88例,其中男54例、女34例,年龄67.6±24.3(28～91)岁。患者为缓慢性心律失常或者严重心力衰竭,放置主动固定电极导线,测定有关参数并随访观察。结果手术顺利完成,未出现严重并发症。共使用主动电极导线151根,其中心室电极导线88根(右室流出道间隔部80根,右室流入道间隔部5根,右室中间隔3根);心房电极63根(右心耳37根,低位房间隔10根,高位房间隔10根,心房侧壁6根)。起搏参数在电极导线置入15min后可达到理想值。术后7天及出院后1,3,6个月随访无电极导线脱位,起搏参数与置入时比较没有差异。结论使用主动固定电极进行心脏特殊部位起搏是可行和安全的。     

三种永久起搏电极慢性阈值的比较

为比较激素电极、靶头电极和螺旋电极的慢性阈值,并探讨其优缺点,对激素电极(26条)、靶头电极(14条)和螺旋电极(20条)的慢性阈值进行了观察。60条电极与单腔或双腔起搏器均系同一公司生产。为提高可比性,仅有5.0 V 电压输出的起搏器不作观察对象。激素电极、非激素电极分别随访18(3～60)和64(3～122)月。结果显示2.5 V 时激素电极的慢性脉宽阈值(0.07±0.03 ms)低于靶头电极(0.11±0.05 ms),后者又低于螺旋电极(0.25±0.13 ms),P 均<0.01。全部病例心房和心室感知均良好。电压输出均采用2.5 V,激素电极、靶头电极和螺旋电极起搏分别置脉宽输出于0.2,0.4和0.8 ms,则80%以上(分别为85%、86%及80%)的病例可达到能量阈值的3倍以上的安全范围。激素电极中有19条可置于1.6 V 和0.3 ms 起搏,其耗能仅为5.0V和0.5 ms(25μJ)的6.1%。即每个脉冲可节能93.9%,从而可延长起搏器的工作寿命。     

Acute effects of cyclosporin and cremophor EL on endothelial function and vascular smooth muscle in the isolated rat heart

Summary We studied the effects of cyclosporin dissolved in the vehicle used as an intravenous preparation, namely, cremophor EL, and cremophor alone on the basal coronary flow plus endothelial function and vascular smooth muscle response by examining their influence on 5-hydroxytryptamine (5-HT) and nitroglycerine (GTN) induced changes in coronary flow in the isolated rat heart. A total of 72 rat hearts were perfused with a modified Langendorf preparation. There was a 12.8±3% reduction in the basal coronary flow after 60 minutes of perfusion with the drug-free buffer (p=ns). A dose of 50 ng/ml of cremophor or cyclosporin gave a similar reduction in the flow (cremophor 9.2±0.7%, cyclosporin 12.7±2%). However, at higher concentrations cremophor caused dose-dependent coronary vasodilation, while cyclosporin had the opposite effect. The maximum effect after 1000 ng/ml of cyclosporin was a 48.7±0.6% decrease, and after an equivalent dose of cremophor a 24.8±2.2% increase in the flow. The vasodilatory response to 5-HT and GTN remained unchanged after 60 minutes of perfusion with the drug-free buffer (5-HT, before 33.3±2.5%, after 37.7±4.2%; GTN, before 34.3±2.5%, after 33.7±1.5%). A period of 60 minutes of perfusion with 500 ng/ml and 1000 ng/ml of cremophor caused a significant reduction in the 5-HT response without an appreciable change in the effect of GTN (500 ng/ml—5-HT, before 29.9±0.9% after 10.7±3.7%; GTN, before 32.3±1.9% after 31.8±3.5%; 1000 ng/ml—5-HT, before 29.7±0.6%, after 12.3±2.7%; GTN, before 33.3±2.8%, after 32.7±1.4%; p<0.001). The same concentration of cyclosporin not only reduced the 5-HT response but also reduced the vasodilation induced by GTN (500 ng/ml—5-HT, before 35.3±3.7%, after 1.6±5%; GTN, before 30.8±1.5%, after 11.2±2.7%; 1000 ng/ml—5-HT, before 32.8±1.9%, after -32.3±1.1%; GTN, before 35.7±0.8%, after 10.0±1.3%). We conclude that cremophor EL causes endothelial dysfunction in the isolated rat heart, and this effect may be aggravated by cyclosporin dissolved in cremophor. Cyclosporin with cremophor also leads to injury to vascular smooth muscle. The direct effect of cremophor is to cause coronary vasodilation, while cyclosporin causes dose-dependent coronary vasoconstriction.     

VVI型起搏器更换时心室电极直接参数的变化及临床意义

研究长期起搏器治疗后起搏阈值、电极阻抗的变化及电极使用的寿命。 32例病人 ,在起搏器置入术及更换术时 ,用起搏器分析仪直接测量心室电极参数。心室电极在体内埋置时间为 10 4 .2 2± 30 .10 (49～ 16 8)个月。置入时起搏阈值为 0 .72± 0 .33(0 .2～ 1.5 )V ,更换脉冲发生器时为 1.85± 0 .75 (1.0～ 3.5 )V ,P <0 .0 0 0 1。更换脉冲发生器时起搏阈值是置入时的 2 .5 7倍 ,增加幅度为 2 0 1.2 %± 16 2 .9% (10 %～ 70 0 % ) ,增加绝对值为 1.13± 0 .71(0 .1～2 .5 )V。置入时电极阻抗为 6 4 2 .83± 185 .39(333～ 980 )Ω ,更换脉冲发生器时为 70 2 .79± 73.0 0 (40 2～ 12 4 0 )Ω ,P >0 .0 5。更换起搏器后 ,对继续使用原心室电极的 2 8例随访 5 4 .91± 5 1.2 1(1～ 16 8)个月。 3例在更换术后 1～ 2 4个月分别出现起搏及感知障碍 ,再次手术时发现导管不全断裂、绝缘包鞘破损及微脱位。结论 :置入性右心室心内膜电极在使用 8年以上 ,大部分的直接参数在正常范围 ,可考虑继续使用 ,但早年生产的电极 ,更换术时参数即使正常 ,亦不排除电极可能短期内发生故障 ,须随访及定期复查。     

Effect of Electrode Length on Atrial Defibrillation Thresholds

Electrode Length for Atrial Defibrillation. Introduction: Catheter-based electrodes have been used previously to terminate episodes of atrial fibrillation in animals and man. Typically, these electrodes span 6 to 7 cm, and lowest energy requirements are achieved when these electrodes are positioned in the distal coronary sinus and in the right atrium. The purpose of this study was to evaluate the use of longer electrode lengths for atrial defibrillation. Methods and Results: In 15 patients, two decapolar catheters were inserted, one into the distal coronary sinus and one in the right atrium. To provide longer electrodes lengths, a third catheter was inserted and alternated positioned in the right atrium or coronary sinus. A 6-cm electrode span was obtained by using the distal 8 rings on the coronary sinus catheter or 8 consecutive electrodes on the right atrial catheter and increased from 6 to 11 cm by connecting consecutive, nonoverlapping rings of the third catheter with the 10 rings of the initial right atrial or coronary sinus catheter. Atrial defibrillation thresholds were determined twice, in a randomized order, in each patient for each of the three combinations of electrode lengths. All 15 patients could he successfully converted to sinus rhythm without complications; however, one patient could be converted reproducibly with only 2 of the 3 electrode combinations. Mean thresholds were 306 ± 102 V, 5.9 ± 4.0 J for the 6 cm/6 cm electrode length combination with an impedance of 72 ± 18 ω. For the electrode combination using the 11-cm electrode in the right atrium, the defibrillation threshold was 296 ± 107 V, 5.8 ± 3.9 J with an impedance of 61 ± 17 ω and was 294 ± 91 V, 5.6 ± 3.6 J with an impedance of 55 ± 11 ω for the 11-cm electrode in the coronary sinus. There were no significant differences in defibrillation voltage or energy (P > 0.05) associated with the longer electrode lengths; however, the longer electrode lengths did significantly lower shock impedance (P < 0.05). Conclusion: The use of longer electrodes, when using the right atrium to coronary sinus shock vector, does not lower the defibrillation requirements for restoration of sinus rhythm.     

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.