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。     

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。     

高脂餐与空腹顿服胺碘酮的药代动力学对比研究

目的　比较空腹和高脂餐后顿服胺碘酮的药代动力学变化 ,探讨饮食对胺碘酮药代动力学的影响。方法　 8名健康男性志愿者 ,年龄 (2 1 6± 1 2 )岁 ,体重 (6 5 8± 5 6 )kg。志愿者分别在空腹12h和进食标准脂肪早餐 (含黄油 1 5 g/kg体重 )后顿服胺碘酮 80 0mg ,两次服药间隔 12周。高效液相色谱法测定胺碘酮及其代谢产物去乙基胺碘酮浓度 ,计算餐后与空腹服药后药代动力学参数及相对生物利用度。结果　结果显示高脂餐后胺碘酮的血浆浓度较空腹服药明显增高。餐后胺碘酮的峰浓度(Cmax)和血药浓度 时间曲线下面积 (AUC0 t)均较空腹服药显著升高 [Cmax(2 330± 12 14)ng/ml对 (90 3± 35 3)ng/ml;AUC0 t(2 72 6 6± 86 6 7)ng·h·ml-1对 (12 82 5± 5 985 )ng·h·ml-1](P <0 0 1) ;消除半衰期 (t1/ 2 )明显延长 [(2 9 6± 9 8)h对 (17 0± 5 3)h](P <0 0 1) ;达到峰值时间 (Tmax)基本不变 [(4 6±1 2 )h对 (4 6± 1 5 )h]。根据各受试者的AUC计算出高脂餐后服药的相对生物利用度为 2 39%±75 %。结论　高脂餐后服药增加胺碘酮的吸收 ,显著增加胺碘酮的血药浓度 ,同时减慢胺碘酮自体内的消除 ,提示进食高脂餐可能影响药物的疗效。     

胺碘酮对心室急性起搏阈值的影响

病态窦房结综合征伴有阵发性心房颤动(房颤)者临床常见，经常需要心脏起搏器与胺碘酮同时治疗。植入起搏器术后即刻起搏阈值不稳定，早期有一定程度的增高，这时使用胺碘酮是否会对心室起搏阈值产生明显影响，尚无文献报道。为此，对18例新近植人心脏起搏器并口服胺碘酮的病人进行心室起搏阈值监测，以期了解胺碘酮对心室急性起搏阈值的影响及其影响程度。     

胺碘酮对起搏器术后快速心律失常的疗效与安全性

目的研究口服胺碘酮对起搏器术后各种快速心律失常的疗效和安全性,为安置人工心脏起搏器后伴发快速心律失常患者口服胺碘酮是否有效和安全提供证据.方法对36例置入永久心脏起搏器并口服胺碘酮治疗快速心律失常的患者进行疗效观察,并跟踪监测心室起搏阈值.另外40例为对照组、监测心室起搏阈值.结果胺碘酮有效率83.3%.术后两组均有心室起搏阈值升高.两组相比较,胺碘酮组较对照组升高更明显.结论胺碘酮对起搏器术后心室起搏阈值有一定影响,但仍在安全范围.     

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。     

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     

胺碘酮与其代谢物去乙基胺碘酮的比较研究

目的　研究健康受试者单剂和连续口服胺碘酮后原形药物和活性代谢物去乙基胺碘酮的药代动力学特点及相互关系。方法　 36例健康男性受试者分两组。单剂量组 2 0例 ,服药 80 0mg/次 ;多剂量组 1 6例 ,服药 60 0～ 80 0mg/d ,连续服药至停药标准。采用反相HPLC方法同时测定受试者胺碘酮和去乙基胺碘酮血药浓度 ,并计算药代动力学参数。主要药代动力学参数比较采用方差分析。结果　 (1 )单剂量组 :胺碘酮和去乙基胺碘酮的达峰时间 (Tmax)分别为 (5 2± 1 5)h和 (8 6± 3 2 )h ,峰浓度 (Cmax)分别为 (0 764± 0 383)mg/L和 (0 1 2 6± 0 0 71 )mg/L ,0至 48h取样的血药浓度 时间曲线下面积 (AUC0 4 8)分别为 (1 0 593± 4 977)mg·h·L- 1 和 (3 936± 1 2 88)mg·h·L- 1 ;(2 )多剂量组 :胺碘酮和去乙基胺碘酮间Tmax和末端消除速率常数 (Ke)差异无显著性 (P >0 0 5) ;其余药代动力学参数Cmax、Tmax、AUC0 4 8等两者之间差异有显著性 (P <0 0 1 )。口服两种负荷剂量后 ,代谢物的各药代动力学参数两组间差异无显著性。结论　无论是单剂或短期连续口服胺碘酮 ,其原形药物、去乙基胺碘酮均存在滞后作用 ,临床给药时应考虑原形药物及其代谢物累积药效的影响     

胺碘酮对预激综合征合并心房颤动患者射频消融时心房颤动发作的预防作用

探讨胺碘酮对预激综合征合并阵发性心房颤动 (简称房颤 )患者房室旁道电生理特性的影响及其在射频消融术中对房颤发作的预防价值。选择有阵发性房颤史的预激综合征患者 4 7例 ,在行射频消融术前 2周口服胺碘酮0 .2g,每日 2次 ;4 5例未服胺碘酮和其他抗心律失常药者作对照组。心电生理检查测定旁道前传、逆传不应期(ERP) ,记录房室折返性心动过速 (AVRT)的诱发率和房颤的发生次数、发作时间及发作时的心室率 ,所有患者均同时行射频消融治疗。结果 :胺碘酮组旁道前传、逆传ERP均较对照组显著延长 ( 3 19± 4 8vs 2 3 5± 2 6ms ;3 0 5± 5 6vs2 4 0± 2 3ms,P均 <0 .0 1)。射频消融术中旁道存在逆传者在两组间无显著差别 ( 85 .1%vs 87.2 %) ,而胺碘酮组房颤的发作次数显著降低 ( 19.1%vs 60 .0 %,P <0 .0 1) ,发作时间显著缩短 ( 8.2± 4 .3vs2 3 .6± 11.7min ,P <0 .0 1) ,房颤发作时的心室率显著减慢 ( 12 7± 2 8vs 165± 3 4次 /分 ,P <0 .0 1) ,胺碘酮组消融治疗成功率与对照组无显著性差异 ( 10 0 %vs 95 .6%,P >0 .0 5 ) ,但手术操作与X线透视时间均显著低于对照组 ( 115 .6± 4 1.2vs 15 3 .1± 5 0 .6min ;3 5 .8± 16.4vs 4 9.3± 2 0 .2min ,P均 <0 .0 1)。结论 :胺碘酮可以有效预防射频消融     

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。     

胺碘酮和普罗帕酮治疗冠心病并室性心律失常的疗效比较

比较胺碘酮和普罗帕酮治疗冠心病心肌缺血患者室性心律失常的疗效。6 9例冠心病心肌缺血合并室性心律失常患者 ,均接受冠心病正规治疗 ,其中 35例同时口服胺碘酮片 (胺碘酮组 ) ,34例口服普罗帕酮片 (普罗帕酮组 ) ,疗程 4周。疗程开始及结束时均行 2 4h动态心电图及 12导联心电图检查。结果 :两组患者用药后 2 4h室性早搏 ,短阵室性心动过速的发作次数均明显减少 (胺碘酮组用药后与用药前比较分别为 2 70 5± 14 77个vs 6 834± 45 2 8个 ,7.4 2± 3.30次vs 1.2 9± 0 .93次 ;普罗帕酮组则分别为 6 712± 3385个vs 396 2± 1983个 ,8.0 5± 3.37次vs4 .2 2± 2 .5 9次 ,P均 <0 .0 1)。胺碘酮组的疗效高于普罗帕酮组 (P <0 .0 1)。两组未见严重副作用。结论 :胺碘酮对冠心病伴室性心律失常的疗效优于普罗帕酮。     

Effect of amiodarone on qt dispersion in the 12-lead standard electrocardiogram and its significance for subsequent arrhythmic events

Background and hypothesis: QT dispersion, measured as interlead variability of QT intervals in the surface electrocardiogram, has been demonstrated to provide an indirect measurement of the inhomogeneity of myocardial repolarization. The purpose of the present study was twofold: (1) to analyze the effect of amiodarone on QT dispersion measured in the 12-lead standard ECG, and (2) to examine the association between QT dispersion on amiodarone and subsequent arrhythmic events. Methods: To determine the effect of amiodarone on QT dispersion and its clinical significance for subsequent arrhythmic events, QT dispersion was measured in the 12-lead standard electrocardiogram (ECG) in 52 patients before and after administration of empiric amiodarone for ventricular tachyarrhythmias. Results: QT intervals increased from 401 ± 44 ms before amiodarone to 442 ± 53 ms after amiodarone therapy, and rate corrected QT intervals (QTc) increased from 452 ± 43 ms to 477 ± 37 ms, respectively (p<0.01). QT dispersion, QTc dispersion, and adjusted QTc dispersion, which take account of the number of leads measured, were not significantly different before and after initiation of amiodarone therapy (58 ± 24 ms vs. 61 ± 26 ms, 68 ± 29 vs. 66 ± 26 ms, and 22 ± 8 vs. 22 ± 8 ms, respectively, p = NS). During 31 ± 25 months follow-up after initiation of amiodarone therapy, arrhythmic events defined as sustained ventricular tachycardia, ventricular fibrillation, or sudden death occurred in 11 of 52 study patients (21%). QT dispersion, QTc dispersion, and adjusted QTc dispersion on amiodarone were not different between patients with and without arrhythmic events during follow-up (65 ± 14 vs. 59 ± 29 ms, 73 ± 15 vs. 64 ± 28 ms, and 25 ± 6 vs. 21 ± 8 ms, respectively, p=NS). Conclusions: We conclude that (1) amiodarone increases QT intervals and QTc intervals during sinus rhythm but does not significantly change measures of QT dispersion; and (2) QT dispersion measured in the 12-lead standard ECG after initiation of amiodarone therapy does not appear to be a useful marker for subsequent arrhythmic events.     

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。     

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.     

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。     

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.     

Amiodarone reduces transmural heterogeneity of repolarization in the human heart

Objectives. The present work was designed to test the effects of amiodarone therapy on action potential characteristics of the three cell types observed in human left ventricular preparations.Background. The electrophysiologic basis for amiodarone’s exceptional antiarrhythmic efficacy and low proarrhythmic profile remains unclear.Methods. We used standard microelectrode techniques to investigate the effects of chronic amiodarone therapy on transmembrane activity of the three predominant cellular subtypes (epicardial, midmyocardial [M] and endocardial cells) spanning the human left ventricle in hearts explanted from normal, heart failure and amiodarone-treated heart failure patients.Results. Tissues isolated from the ventricles of heart failure patients receiving chronic amiodarone therapy displayed M cell action potential duration (404 ± 12 ms) significantly briefer (p < 0.05) than that recorded in tissues isolated from normal hearts (439 ± 22 ms) or from heart failure patients not treated with amiodarone (449 ± 18 ms). Endocardial cells from amiodarone-treated heart failure patients displayed longer (p < 0.05) action potential duration (363 ± 10 ms) than endocardial cells isolated from normal hearts (330 ± 6 ms). As a consequence, the heterogeneity of ventricular repolarization in tissues from patients treated with amiodarone was considerably smaller than in the two other groups, especially at long pacing cycle lengths.Conclusions. These findings may explain, at least in part, the reduction of ventricular repolarization dispersion and the lower incidence of torsade de pointes observed with chronic amiodarone therapy as compared with other class III agents.