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。     

静脉注射利多卡因对慢性期心室起博阈值的影响

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。     

胺碘酮对心室慢性起搏阈值的影响

为探讨胺碘酮对心室慢性起搏阈值的影响 ,对 12例安置心脏起搏器 3个月后伴发症状性心律失常患者 ,予胺碘酮治疗 ,用相应的程控仪测试用药前后的起搏阈值。药前 ,药后 1h、4h、1周和 2周的起搏阈值 (输出固定为2 .5V)分别为 0 .0 8± 0 .0 2 ,0 .0 8± 0 .0 1,0 .0 7± 0 .0 2 ,0 .0 8± 0 .0 1和 0 .0 8± 0 .0 2ms(P >0 .0 5 )。结论 :胺碘酮对心室慢性起搏阈值无影响。     

植入性心脏起搏器更换时心室电极直接参数的变化

分析了本院 90年代以来更换起搏脉冲发生器时心室电极参数的直接测量结果。在 2 6例病人中 ,男 15例、女 11例 ,年龄 6 3 .9± 13.6 ( 19～ 90 )岁。Ⅲ度房室阻滞 14例、病窦综合征 12例。在更换手术中 ,应用起搏分析仪直接测量原心室起搏电极参数。结果 :至测量时原心室起搏电极在体内埋置时间为 114.2± 2 7.4( 5 8～ 179)个月。首次埋置时的起搏阈值为 0 .5 9± 0 .2 7V ,更换脉冲发生器时为 1.6 0± 0 .75V(P <0 .0 0 0 1) ,起搏阈值增加的幅度为198.1%± 141.1% ( 2 0 %～ 5 6 7% ) ,增加的绝对值为 1.0± 0 .7( 0 .1～ 3 .0 )V。更换脉冲发生器时 ,起搏电极阻抗 5 5 8.5± 136 .3Ω。更换起搏脉冲发生器后 ,继续使用原心室起搏电极 2 2例。术后随访 48.7± 30 .6 ( 6～ 96 )个月。 2例于更换术后 12 ,2 4个月 (即原心室起搏电极在体内埋置时间分别为 98,12 0个月 )分别出现起搏器感知功能不良。重新手术时发现 ,原心室电极起搏阈值或阻抗增高。其余病人起搏与感知功能均良好。结论 :植入性心室起搏电极使用约 10年后 ,大部分电极的直接测量参数仍在良好范围 ,可以考虑继续使用 ,但必须注意随访 ,定期复查     

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。     

右室双部位起搏治疗心力衰竭的临床观察

评价 15例患者经右室双部位起搏治疗慢性心力衰竭 (简称心衰 )的疗效。其中原发性扩张型心肌病心衰 13例、缺血性心肌病心衰 2例 ;心功能Ⅲ级 9例、Ⅳ级 6例。结果 :15例患者安置时右室心尖部起搏阈值 0 .5± 0 .3(0 .3～ 1.0 )V、R波振幅 15± 5 .98(6～ 2 4.6 )mV ,阻抗 6 13± 172 (32 0～ 90 0 )Ω。右室流出道起搏阈值 0 .7± 0 .2 6 (0 .3～1.3)V、R波振幅 13± 5 .5 5 (6 .5～ 2 3.6 )mV、阻抗 5 6 3± 194(30 0～ 90 0 )Ω ;双部位起搏阈值 1.45± 0 .45 (0 .9～ 1.7)V。双部位起搏心电图QRS波群时限比右室心尖部及右室流出道单部位起搏缩短了 40～ 90ms。超声心动图检查提示双部位起搏后二尖瓣返流面积平均减少 5 .6cm2 ,射血分数值提高 5 .2 %。经 6 .0± 1.5个月的随访 ,15例中除 2例因突发恶性室性心律失常猝死外 ,其余患者的心功能分别从Ⅲ、Ⅳ级改善到Ⅱ和Ⅲ级。右室双部位慢性起搏阈值1.85± 0 .5 6 (1.5～ 2 .5 )V。随访期间QRS波群时限平均下降 5 0ms。结论 :右室双部位起搏能有效的治疗心肌病患者的心衰。     

InSync 8040起搏器在充血性心力衰竭治疗中的初步应用

观察InSync 80 40起搏器治疗扩张型心肌病 (DCM)伴充血性心力衰竭 (CHF)的疗效。 8例DCM伴CHF患者 ,男 7例、女 1例。其中伴完全性左束支阻滞 6例 ,左前分支阻滞、右室起搏后宽QRS波 (>0 .2 0s)各 1例。通过冠状静脉窦置入 2 187电极起搏左室 ,右房电极和左、右室电极分别与InSync 80 40起搏器A、V1、V2 孔相连接。术后起搏阈值 3.75± 0 .6 (3.0～ 5 .0 )V。患者CHF的症状明显改善 ,术后左室舒张末径、左室射血分数、左室短轴缩短率、心胸比例较术前均有改善 (分别为 6 6 .1± 6 .93mmvs 72 .5± 8.1mm、0 .374± 0 .0 31vs 0 .2 81± 0 .0 5 3、19.8%± 2 .2 %vs12 .2 %± 2 .7%、0 .5 9± 0 .4vs 0 .6 4± 0 .2 0 ;P均 <0 .0 5 )。结论 :初步临床应用表明 ,以InSync 80 40起搏器行双心室同步起搏治疗CHF疗效肯定     

遥测技术对预测和延长起搏器寿命的临床意义

目的：为选择长期有效和适宜的低起搏器输出，方法：23倒心动过缓患者檀人起搏器Minix 2台，Prevail2台及Premier19台．激素电极4023型4条和4003型19条。用9710E程控器(Medtronic)以手控测阈值法和遥测技术(RTT)随访慢性起搏阈值，平均电池耗电(μA)和脉冲瞻量输出(μ)等参数3～27个月以上。结果：1．6V和0．8V的慢性起搏脉宽阈值分别为0.11±0．04(0．06～0．18)ms和0．20±0．08(0．12～0．42)ms．并发现1．6V和2倍于其脉宽阈值起搏的电池耗电量(5．45±0．59μA)比0．8v和3倍于其脉宽阈值起搏的5．96±0.88μA更低(P<0.05)而1.6V起搏的脉冲能量输出(1．74±0．53μJ)则比0．8V起搏(0．92±0．40μJ)更大（P<0.001)。设置1.6V和其脒宽阈值的2倍(脉宽阈值0．06ms时置于0．18ms)的平均安全范围(能量输出／能量阈值)为5.6倍,随访16～40个月证明起搏良好，预期平均寿命为21.2±2．13年，均明显优于设置输出为0.8V和3倍于其脉宽阈值的工作寿命(19．5±2．65年)及其安全范围(3倍)。结论：本结果提示起搏器输出1．6V比0．8V的预期起搏器寿命更长(21．2比19．5年)．且其平均安全范围更大(5．6比3.0)。     

植入起搏电极参数的测定和随访

为了解起搏阈值、起搏阻抗和感知阈值的变化，对４２根心房电极和４９根心室电极进行了随访。结果显示：心房电极慢性期起搏阈值为１．１７±０．３５Ｖ／０．５ｍｓ，出现波动者６例（２７．３％），心室电极为１．２７±０．３８Ｖ／０．５ｍｓ，出现波动者７例（３０．４％）；１９根电极的起搏阻抗在急性期均有波动，慢性期为５８５．６±１５０Ω，慢性期出现波动者２例（１０．５％）；１１根心房电极慢性期感知阈值（Ｐ波振幅）与植入时相一致。     

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。     

心房起搏阈值的随访分析

对３３例植入心房电极者进行起搏阈值的随访，结果表明：起搏阈值峰值为１．４４±０．７４Ｖ／０．５ｍｓ，出现在植入后两周内；慢性期起搏阈值为１．２２±０．４０Ｖ／０．５ｍｓ；伴器质性心脏病患者慢性期起搏阈值（１．７０士０．３７Ｖ／０．５ｍｓ）明显高于不伴器质性心脏病者（１．１６±０．３７Ｖ／０．５ｍｓ），Ｐ＜０．０１；激素电极的起搏阈值峰值（１．１２±０．２９Ｖ／０．５ｍｓ）和慢性期起搏阈值（０．７７±０．１７Ｖ／０．５ｍｓ）均显著低于非激素电极（１．８０±０．６８Ｖ／０．５ｍｓ和１．４０±０．３３Ｖ／０．５ｍｓ），Ｐ＜０．０５及０．００１。提出在非特殊情况下，将出厂时的电能由５．０Ｖ／０．５ｍｓ降至２．５Ｖ／０．５ｍｓ既可保证有效起搏，又可节省电能，从而延长起搏器的使用寿命。     

右房左室起搏治疗慢性心力衰竭伴室内传导阻滞患者的初步临床观察

观察右房 左室起搏治疗慢性心力衰竭 (简称心衰 )的临床效果。选择 1 6例充血性心衰患者 (NYHA分级Ⅲ Ⅳ级 ) ,男 1 0例、女 6例 ,年龄 6 8.4± 6岁 ;均为窦性心律 ,合并有Ⅰ度房室阻滞 ,完全性左束支阻滞。按安置起搏器的模式分为右房 左室起搏治疗组 (LV组 ,n =6 ) ,右房双室起搏治疗组 (BiV组 ,n =1 0 )。左室起搏电极分别放置于心大静脉左室侧后分支 9例 ,心大静脉左室后分支 7例。观察起搏治疗前后左室心功能参数、6min步行距离、左室壁运动的同步性及体表心电图的变化。结果 :BiV组左室射血分数 (LVEF)由术前的 0 .2 3提高至 0 .31 (P <0 .0 0 1 ) ;在LV组LVEF由术前的 0 .2 4提高至 0 .33(P <0 .0 0 1 ) ;左室舒张末期容积指数在二组分别由术前的 1 4 9± 5 1ml/m2 和 1 5 3±5 3ml/m2 下降至 1 1 6± 38ml/m2 和 1 2 1± 4 1ml/m2 (P均 <0 .0 0 1 ) ;室间隔与左室后壁运动的延迟时间在二组分别由术前的 1 95± 94ms和 1 97± 89ms下降至 1 7± 6 0ms及 1 6± 5 6ms(P均 <0 .0 0 1 )。 6min步行距离则分别由术前的4 0 3± 5 3m和 4 0 1± 5 9m提高至 4 4 1± 6 2m和 4 4 2± 6 7m(P均 <0 .0 5 )。结论 :初步临床观察提示右房 左室起搏治疗与右房双室起搏治疗相比 ,同样可有效地改善慢性心衰?     

Effect of digoxin on coronary blood flow and myocardial oxygen consumption in patients with chronic coronary artery disease

In 10 patients with chronic coronary artery disease and without clinical evidence of congestive heart failure, the effects of 1.0 mg of digoxin intravenously on systemic hemodynamics, coronary blood flow, myocardial oxygen consumption and myocardial lactate extraction were studied both at rest and during atrial pacing. Atrial stimulation at a rate just below the threshold for angina led to a significant decrease in left ventricular enddiastolic pressure, from 10.6 ± 1.6 to 7.1 ± 0.8 mm Hg, associated with a significant decrease in left ventricular stroke work index per beat, from 76.7 ± 5.11 to 40.3 ± 4.01 g-m/m². After digoxin, nearly identical results in stroke work index could be observed at rest and during stimulation (75.2 ± 6.74 and 44.1 ± 5.92, respectively). However, left ventricular enddiastolic pressure decreased significantly before and during atrial stimulation (8.1 ± 1.29 and 4.7 ± 1.09 mm Hg, respectively). Cardiac index decreased from 3.08 ± 0.20 to 2.73 ±0.17 liters/min per m² at rest but during pacing it no longer differed before and after digoxin (3.17 ± 0.22 and 3.10 ± 0.20 liters/min per m², respectively). Myocardial oxygen consumption and lactate extraction remained unchanged after digoxin both at rest and during atrial pacing.It is concluded that some deficiency in left ventricular function is present in patients with chronic coronary artery disease even without clinical evidence of congestive heart failure. Digoxin improves left ventricular performance at rest and during stress conditions. An expected increase in myocardial oxygen consumption due to enhanced contractility is completely counterbalanced, probably by a decrease in left ventricular volume after digoxin.     

Transvenous versus open chest lead placement for resynchronization therapy in patients with heart failure: comparison of ventricular electromechanical synchronicity

Background Transvenous lead placement is the standard approach for left ventricular (LV) pacing in cardiac resynchronization therapy (CRT), while the open chest access epicardial lead placement is currently the most frequently used second choice. Our study aimed to compare the ventricular electromechanical synchronicity in patients with heart failure after CRT with these two different LV pacing techniques. Methods We enrolled 33 consecutive patients with refractory heart failure secondly to dilated cardiomyopathy who were eligible for CRT in this study. Nineteen patients received transvenous (TV group) while 14 received open chest (OP group) LV lead pacing. Intra- and inter-ventricular electromechanical synchronicity was assessed by tissue Doppler imaging (TDI) before and one year after CRT procedure. Results Before CRT procedure, the mean QRS-duration, maximum time difference to systolic peak velocity among 12 left ventricle segments (LV Ts-12), standard deviation of time difference to systolic peak velocity of 12 left ventricle segments (LV Ts-SD), and inter-ventricular mechanical delay (IVMD) in OP and TV group were 166 ± 17 ms and 170 ± 21 ms, 391 ± 42 ms and 397 ± 36 ms, 144 ± 30 ms and 148 ± 22 ms, 58 ± 25 ms and 60 ± 36 ms, respectively (all P > 0.05). At one year after the CRT, the mean QRS-duration, LV Ts-12, LV Ts-SD, and IVMD in TV and OP group were 128 ± 14 ms and 141 ± 22 ms (P = 0.031), 136 ± 37 ms and 294 ± 119 ms (P = 0.023), 50 ± 22 ms and 96 ± 34 ms (P = 0.015), 27 ± 11 ms and 27 ± 26 ms (P = 0.86), respectively. The LV lead implantation procedure time was 53.4 ± 16.3 min for OP group and 136 ± 35.1 min for TV group (P = 0.016). The mean LV pacing threshold increased significantly from 1.7 ± 0.6 V/0.5 ms to 2.3 ± 1.6 V/0.5 ms (P < 0.05) in TV group while it remained stable in the OP group. Conclusions Compared to conventional endovascular approach, open chest access of LV pacing for CRT leads to better improvement of the intraventricular synchronization.     

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.     

Electrophysiologic and hemodynamic effects of propafenone,a new antiarrhythmic agent,on the anesthetized,closed-chest dog: Comparative study with lidocaine

The relative hemodynamic and electrophysiologic effects of a new antiarrhythmic drug, propafenone, and lidocaine were evaluated in eight closed-chest, anesthetized dogs. Propafenone (4 mg/kg intravenously) significantly (p < 0.05) lowered aortic and pulmonary systolic pressures and caused a rise in heart rate (p < 0.05). Cardiac output decreased from 4.5 ± 1 to 3.8 ± 0.7 L/min (p < 0.05) during atrial pacing at 400 msec cycle length. Propafenone had no effect on pulmonary and aortic diastolic pressures. Lidocaine (5 mg/kg intravenously) caused a significant (p < 0.05) decrease in aortic systolic pressure and a rise in heart rate. Lidocaine had no significant effect on the other measured hemodynamic parameters. Propafenone, unlike lidocaine, significantly (p < 0.05) increased atrioventricular nodal functional refractory period and right ventricular endocardial (apex) cathodal (0.5 ± 0.1 mA to 1.9 ± 0.3 mA) and bipolar (1.4 ± 0.3 to 2.2 ± 0.4 mA) diastolic excitability threshold. Propafenone, unlike lidocaine, also caused a significant (p = 0.05) intraatrial conduction delay; however, neither drug caused conduction slowing in the His-Purkinje system. Both drugs had no effect on sinus nodal recovery time and on the effective refractory period of the right ventricular endocardium (apex). Mean plasma propafenone levels during hemodynamic and electrophysiologic measurement ranged between 3.2 ± 1.8 μg/ml and 1.7 ± 1.1 μg/ml. All of the propafenone-induced effects were reversible within 90 minutes. We conclude that propafenone differs from lidocaine in its atrial, AV nodal, and ventricular electrophysiologic properties, and thus these may explain propafenone's greater efficacy over lidocaine against both certain atrial and ventricular arrhythmias. Propafenone's negative inotropic effects, however, should necessitate caution in its use.