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。     

植入式电极导线和临时起搏电极导线行临时心脏起搏的比较

目的比较植入式电极导线和临时起搏电极导线行临时心脏起搏(TCP)的效果。方法选择在本院行TCP的患者33例分为研究组(n=19)和对照组(n=14)。研究组采用植入式电极导线外接永久起搏器行TCP;对照组采用传统临时起搏电极导线行TCP。比较两种导线行TCP的阈值、脱位率及总费用。结果研究组10例使用主动电极导线,9例使用翼状被动电极导线,未发生脱位,对照组使用电极导线为(BARD0071539,6F型),脱位4例,均经重新定位。两组TCP 24h后的起搏阈值无明显差异(P>0.05)。研究组TCP术后住CCU病房的时间少于对照组[(0.6±0.4)d vs(3.2±1.3)d](P<0.05),总费用少于对照组[(4 587±398)元vs(7 636±567)元](P<0.05)。结论应用植入式电极导线比临时起搏电极导线行TCP更安全、实用、经济。     

心室主动固定电极导线固定时损伤电流特征分析

目的探讨主动固定电极导线植入心肌后急性损伤电流（COI）的特征及持续时间,指导COI在临床上使用。方法对59例首次植入起搏器患者植入心室主动固定电极导线时,用Medtronic 2290起搏器分析仪测定旋前;旋后1,5,10 min的COI,打印出来并记录。结果一共尝试66次,59次固定稳定及阈值良好,7次旋后出现高阈值或急性脱位。心室主动固定电极导线固定稳定且阈值良好时,55例（93.2%）在旋后1 min有COI,54例（91.5%）在旋后5 min有COI,50例（84.7%）旋后10 min仍有COI。而旋后1 min出现高阈值或急性脱位时,旋后1min均无COI（P〈0.001）,ST80均≤0 mV（P〈0.001）。结论主动固定电极导线螺旋旋出后固定稳定及阈值良好时,旋后1 min可见到明显COI,并可持续10 min以上,而电极导线急性脱位或阈值较高时,旋后1 min无COI或ST80≤0 mV。     

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。     

永久心脏起搏电极导线在临时心脏起搏中的实用性和成本效益

目的 探讨应用永久心脏起搏电极导线连接外置可重复使用的永久起搏器进行临时心脏起搏（TCP）的实用性和成本效益。方法 将具有TCP适应证的48位患者分为研究组（n=18）和对照组（n=30）。 研究组应用永久心脏起搏电极导线连接外置可重复使用的永久起搏器进行TCP;对照组进行传统方法TCP。 结果 研究组18例及对照组30例患者均成功地进行了TCP。研究组中有6例采用了主动螺旋起搏电极导线,另外12例应用翼状被动起搏电极导线。 研究组因为可逆性原因所致心动过缓进行TCP的比例（10 /18）高于对照组（8 /30）;而因永久起搏器植入前保护性TCP的比例（3/18）小于对照组（16/30）（P〈0.05）。 研究组患者全部而对照组仅有17%经锁骨下静脉途径进行TCP（P〈0.05）。 研究组TCP应用时间长于对照组[（7.9±6.5）d vs （3.9±2.3）d,P〈0.05]。 研究组因TCP而住CCU病房的时间短于对照组[（0.2±0.5）d vs （2.6±1.2）d,P〈0.05]。 对照组起搏电极导线脱位33次而研究组无脱位。 对照组有1例患者发生心包压塞。 两组与TCP相关的总医疗花费相当（未计算起搏器费用）。 结论 应用永久心脏起搏电极导线连接外置可重复使用的永久起搏器进行TCP,实用性强且不增加医疗经费。     

心脏起搏主动与被动电极导线的拔除难度对比研究

目的 探究心脏起搏主动与被动电极导线在拔除的手术时间和并发症上是否存在差异。方法 选取新疆医科大学第一附属医院从2016年1月至2022年6月进行电极导线拔除的病人共109例,去除除颤电极导线患者8例,未使用工具拔除患者54例,剩余47例,共77根电极导线,其中主动电极导线31根,被动电极导线46根,其中22根使用锚定钢丝拔除,55根使用针眼圈套器拔除。比较两种电极导线之间的手术时间和并发症情况。结果 两组患者的年龄、性别、基础疾病、拔除原因无明显差异。在未进行电极导线使用年限匹配的情况下,主动电极导线的拔除时间明显减少[(46.74±17.95)min vs(56.41±19.61)min,P=0.031],心房主动电极导线的拔除时间较被动电极导线明显缩短[(30.42±10.84)min vs(52.90±19.82)min,P=0.009],在心室电极导线中,两种电极导线的拔除时间无明显差异[(51.50±16.89)min vs(59.36±19.34)min,P=0.137]。主动电极导线的使用年限较短[(4.60±3.64)年vs(10.27±4.26)年,P<0.0...     

起搏电极导线脱位

起搏电极导线脱位是起搏器术后常见的并发症。大多为发生在起搏器术后6周内的早期脱位,心房电极和双室同步起搏的冠状窦电极的脱位率较高。诊断电极脱位最简便、有效的检查是心电图和X线片,对疑诊患者,应进行起搏器程控。典型的电极导线脱位表现为起搏阈值升高和/或电极导线阻抗降低,严重脱位尚可引起感知不良。根据起搏器置入的时间、患者临床表现、脱位的电极导线情况以及起搏器功能障碍的程度不同,处理方法亦不同,而积极预防是最好的防治电极导线脱位的方法。     

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。     

不同永久起搏电极植入右心室心尖部的损伤电流变化

目的 探讨不同永久起搏电极植入右心室心尖部后损伤电流（current of injury,COI）的变化特点。方法 入选144例右心室心尖部植入永久起搏电极患者,分为被动电极组及主动电极组。测定电极固定后0、5和10 min的COI及常规起搏参数,分析COI变化特点。结果 被动电极固定后0、5和10 min分别测定COI值均明显小于主动电极固定后测定的COI值（P<0.01）。两种电极固定后COI随时间均显著逐步下降（P<0.01）,被动电极固定后COI值下降幅度明显大于主动电极（P<0.01）。被动电极固定后10 min内后5 min COI下降幅度大于前5 min下降幅度（P<0.01）,主动电极固定10 min内COI值前后5 min下降幅度未见差异。术后3例患者电极脱位,其COI均<5.0 mV。结论 右心室心尖部植入被动电极产生的COI明显小于主动电极,两种电极产生的COI均随时间逐步减小,被动电极产生的COI下降速度较快。     

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。     

不同起搏导线植入术中的损伤电流特征

目的明确不同起搏导线在植入过程中产生的损伤电流（COI）形态及变化特征。方法经起搏分析仪及体表心电图仪同步记录右心室螺旋及翼状导线、左心室心脏静脉导线及埋植多年的右心室起搏导线产生的腔内心电图（ICEG）,动态观察其形态及COI变化特征。COI大小指标包括J点后80ms处的ST段振幅（ST80）,ST80与自身R波振幅之比（ST80／R）以及ICEG时限（IED）。结果共记录81根起搏导线的ICEG,包括48根螺旋导线、21根翼状导线、6根左心室心脏静脉导线和6根埋植多年的起搏导线。两种方法均记录到螺旋及翼状导线产生的COI;起搏分析仪描记的螺旋导线固定10min的sT80[（7．7±2．7）mV对（5．1±0．6）mV],ST50／R[（0．62±0．24）对（0．54±0．07）]及IED[（233．6±33．7）ITIS对（211．5±29．3）ms]与固定0min相比,差异无统计学意义（P〉0．05）;而翼状导线固定10min的ST80[（5．6±2．8）mV对（0．8±0．6）mV,P〈0．01],ST80／R[（0．39±0．12）对（0．01±0．01）,P〈0．os3及IED[（145．4±79．4）ms对（64．3±19．8）ms,P〈0．01）]与固定0min相比大幅减小,且大部分时间点的ST孙ST80／R值均较螺旋导线的相应值小（P〈0．05）。总体上,体表心电图仪记录到相似的COI变化趋势。左心室心脏静脉导线及埋植多年的起搏导线均无CO／产生。结论螺旋导线与翼状导线相比,COI值较大,持续时间较长。左心室心脏静脉导线及埋植多年的起搏导线不产生COI。     

Negative current of injury due to inadvertent polarity reversal during active atrial lead implantation

We report an example of the negative current of injury (COI) during permanent pacemaker implantation. Cardiac perforation was our first priority. However, patient had stable hemodynamics, and the fluoroscopic location of the atrial lead was acceptable. Therefore, the connections were checked revealing the cause of the negative COI; the red (+) clips was attached to the tip of the atrial lead rather than anodal ring. Correcting the connections resolved the problem. This report shows that a negative COI might not only be due to cardiac perforation or right ventricular ischemia but that checking the lead connectivity should be carried out first.     

Effect of locally released catecholamines on lipolysis and injury of the hypoxic isolated rabbit heart

The ability of endogenous myocardial catecholamines to stimulate lipolysis of endogenous triglycerides and the role of this process in the development of myocardial injury were studied in isolated, Langendorff-perfused rabbit heart preparations exposed to 3 h of hypoxic perfusion followed by 30 min of aerobic perfusion.Untreated hearts responded not only to hypoxia but also to reoxygenation with surges of noradrenaline outflow lasting 10 and 5 min, respectively. During hypoxia but not during reoxygenation a parallel surge of glycerol outflow was observed. Nicotinic acid (10^?5m) prevented glycerol outflow during hypoxia but did not influence the outflow of noradrenaline during either hypoxia or reoxygenation. Neither noradrenaline nor glycerol were detected in the effluent from the hearts depleted of endogenous catecholamines by reserpine pretreatment. Those hearts also showed a smaller lactate dehydrogenase release during hypoxia (49% reduction) and no increase in lactate dehydrogenase release during reoxygenation. Similar reduction of lactate dehydrogenase release during hypoxia (52% reduction) was observed in the hearts treated with nicotinic acid. This drug, however, did not prevent the reoxygenation-induced lactate dehydrogenase release. The effects of reserpinization and nicotinic acid treatment on lactate dehydrogenase release were not additive.It is concluded that hypoxia is a stimulus for lipolysis in the isolated rabbit heart and most probably this process is catecholamine dependent. At least part of the deleterious effect of endogenous catecholmines on hypoxic myocardium might be attributed to catecholamine-stimulated lipolysis of endogenous triglycerides. The latter, however, does not seem to contribute to deleterious effects of endogenous catecholamines during reoxygenation.     

超声指导下心脏再同步治疗后参数优化的研究

目的探讨如何进行参数优化以提高心脏再同步化治疗(CRT)疗效。方法对8例慢性心力衰竭CRT患者,术后在超声心动图指导下优化AV间期,在组织多普勒显像下优化VV间期,达到CRT最佳治疗目的。结果8例CRT后心功能都得到改善,心功能NYHA分级,从Ⅲ～Ⅳ级改善为Ⅱ～Ⅲ级,起搏时的AV间期与窦性心律时的AV间期之比优化至130～180/100～150ms,使得左室充盈时间从354±147ms升至420±112ms,二尖瓣返流由8.41±4.55cm2减少至5.36±4.71cm2;VV间期优化至4～40ms,使得左室内各室壁收缩期达峰时间标准差从48.4±17.9ms减少至30.2±18.6ms,左室流出道速度时间积分由20.6±9.0cm/s上升至26.1±3.1cm/s。结论术后个体化的参数优化可以提高CRT疗效。     

Relation between lipolysis and glycolysis during ischemia in the isolated rat heart

Summary The relation between lipolysis and glycolysis during ischemia was investigated in isolated perfused rat hearts. In hearts perfused with 11 mM glucose, ischemia caused a marked increase of glycerol release from 10 to 33 nmol/g wt weight/min. Substrate-free perfusion induced an initial stimulation of glycerol release, but lipolysis was subsequently reduced to values comparable to normoxic conditions. Neither did perfusion in the presence of acetate (10 mM) and -hydroxybutyrate (10 mM) stimulate lipolysis. Inhibition of glycolysis by pyruvate prevented the increase of glycerol release during ischemia. These data suggest a tight link between glycolysis and lipolysis during ischemia which is probably mediated by the availability of glycolytically produced glycerol-3-phosphate for reesterification. In the absence of glycerol-3-phosphate, the lipolysis is regulated by product inhibition. As a consequence, the tissue triglyceride levels after perfusion remained fairly constant in all groups of hearts.The calculated energy loss by the reesterification cycle during ischemia was found to be approximately 2.5% of the total energy production. These data are inconsistent with the assumption that this energy loss contributes significantly to the negative energetic balance of the heart during ischemia. Removal of fatty acids by reesterification may constitute a protective mechanism in order to prevent excessive intracellular accumulation of fatty acids and derivative esters during ischemia.     

黄芪及其活性成分对离体豚鼠心脏的作用

目的 探讨黄芪及其活性成分黄芪总黄酮、黄芪总皂苷、黄芪多糖对豚鼠离体心脏心肌缺血再灌注损伤的影响.方法 将36只豚鼠的离体心脏分为正常对照组(对照组)、缺血再灌注组(模型组)、黄芪组(AST组)、黄芪总黄酮组(TFA组)、黄芪总皂苷组(TSA组)和黄芪多糖组(APS组)6组.检测豚鼠离体心脏的心率、冠状动脉流量、心肌梗死面积、灌流液中乳酸脱氢酶(LDH)和肌酸激酶(CK)的活性、心肌组织中丙二醛(MDA)含量和超氧化物歧化酶(SOD)的活性等.结果 再灌注期各时间点模型组心率均较对照组相应的时间点低(P ＜0.05或0.01),AST组和TFA组则均较模型组高(P ＜0.05或0.01),TSA组和APS组心率没有明显改善.再灌注5、10、15、20、25、30、40、50、60 min时模型组冠状动脉流量均较对照组相应时间点低(P均＜0.01).再灌注期AST组冠状动脉流量均高于模型组(P＜0.05或0.01).再灌注5、10、25、30、40 min时TFA组冠状动脉流量均高于模型组(P ＜0.05或0.01).TSA组和APS组冠状动脉流量没有明显改善.再灌注15、25、40、60 min时模型组灌流液中LDH活力均高于对照组(P均＜0.01).再灌注15、25、40、60 min时AST组灌流液中LDH活力均低于模型组(P均＜0.01).再灌注5、15、25、40、60 min时TFA组灌流液中LDH活力均低于模型组(P＜0.05或0.01).再灌注5 min时APS组灌流液中LDH活力显著低于模型组(P＜0.05).再灌注后各时间点TSA组灌流液中LDH活力与模型组比较差异均无统计学意义.再灌注15、60 min时模型组灌流液中CK活力均高于对照组(P均＜0.01).再灌注15 min时AST组和TFA组灌流液中CK活性均低于模型组(P均＜0.01).再灌注60 min时模型组灌流液中CK活力显著高于对照组(P＜0.01).AST组与TFA组灌流液中CK活力分别均低于模型组(P值分别为0.008和0.015).模型组缺血再灌注心肌组织中MDA含量为(5.95±0.91) μmol/g蛋白高于对照组的(3.62±0.58) μmol/g蛋白(P＜0.01).AST组和TFA组心肌组织中MDA含量分别为(4.52 ±0.47)和(4.47±0.78)μmol/g蛋白,均低于模型组(P分别＜0.01和0.05).模型组缺血再灌注心肌组织中SOD活力为(98.64±12.49) U/mg蛋白低于对照组的(153.55±13.25) U/mg蛋白(P＜0.01).AST组和TFA组心肌组织中SOD活力分别为(130.73 ±14.85)和(124.38±13.35) U/mg蛋白,均高于模型组(P均＜0.01).模型组心肌梗死面积百分比为(18.9±2.27)％高于对照组的(1.60±0.33)％(P＜0.01).AST组和TFA组心肌梗死面积百分比分别为(11.9±2.03)％和(13.31±1.17)％,均低于模型组(P均＜0.01).结论 黄芪及其有效成分黄芪总黄酮对豚鼠离体心脏心肌缺血再灌注损伤有保护作用,其机制可能与抗氧化应激有关.     

Clofilium in the isolated perfused rabbit heart: A new model to study proarrhythmia induced by class III antiarrhythmic drugs

Objective: The clinical usefulness of class III antiarrhythmic drugs for the treatment of tachyarrhythmias is limited by their potential proarrhythmic effects, mainly torsades-depointes (TdP). The goal of this experimental study was to develop an isolated whole-heart model exhibiting typical characteristics of class III drug-induced ventricular arrhythmias. Methods: Isolated rabbit hearts were perfused with a Krebs-Henseleit buffer containing 10 μM clofilium and then exposed to a modified Krebs-Henseleit buffer with 2.0 mM K² and 0.5 mM Mg²⁺. Hearts subjected to either clofilium alone or modified buffer alone were used as controls. Results: Under clofilium the QT interval increased from 187±16 to 282±33 ms. Within 8 to 25 s after the change of the perfusate, ventricular arrhythmias developed in all hearts associated with a further QT prolongation to 380±73 ms when the first ventricular extrasystole occurred. Simultaneously, the monophasic action potential durations increased relatively more during late repolarization; from 99±21 to 110±25 ms (+11%) at 50% repolarization, from 143±24 to 178±40 ms (+24%) at 70%, and from 200±30 to 275±53 ms (+38%) at 90%. The predominant rhythm was polymorphic with either two alternating or multiple QRS morphologies exhibiting the characteristic features of torsades-depointes. All control hearts stayed in normal sinus rhythm. Conclusion: Under the conditions selected, the isolated perfused rabbit heart represents a useful experimental approach to study the proarrhythmic effects of class III agents. This model provides a convenient way to manipulate the ionic and pharmacologic millieu in a preparation conserving the functional anatomy of the whole organ without interference by cardiovascular reflexes. It might be useful for analyzing the conditions favoring and preventing drug-induced torsades-depointes. Received: 13 August 1997, Returned for revision: 10 September 1997, Revision received: 29 September 1997, Accepted: 22 October 1997     

Experimental myocardial infarction with left ventricular failure in the isolated perfused rat heart. Effects of isoproterenol and pacing.

Within one minute of acute coronary artery occlusion in the isolated rat heart performing external mechanical work, cardiac output and left ventricular peak systolic pressure fell by one-third to onequarter and there were decreases in the contents of ATP and phosphocreatine (CP) in the ischaemic tissue. Left ventricular and diastolic pressure rose, and $\text{d}\text{p}\text{d}\text{t}{}_{\mathrm{<mtext>max</mtext>}}$ fell. Cardiac output was steady for 60 min post-ligation. The size of infarction was quantified by the use of radioactive microspheres; over one-half of the left ventricle was rendered ischaemic. There was a biphasic response to dl-isoprenaline HCl (10^?6m) added to the perfusate. A temporary increase in cardiac output was followed by a rapid decrease as the heart rate exceeded about 350/min, although $\text{d}\text{p}\text{d}\text{t}{}_{\mathrm{<mtext>max</mtext>}}$ increased throughout. When the heart rate was fixed by pacing, isoproterenol was able to double stroke volume and $\text{d}\text{p}\text{d}\text{t}{}_{\mathrm{<mtext>max</mtext>}}$, coronary flow rose by about one-third. Thus in this model the positive inotropic effect of isoproterenol on the ischaemic myocardium became masked as a negative contribution associated with a concomitant chronotropic effect developed. There was also a negative effect of pacing on the cardiac output of non-ligated hearts, but the magnitude was less. It is proposed that a fixed coronary flow rate limited the oxygen delivery to the myocardium as the heart rate rose.