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1.
目的研究已经证实心外膜起搏可引起离体心脏心室肌跨壁离散明显增加,双心室同步治疗中室性恶性心律失常的增加可能是由于左心室起搏增加心室肌复极离散,然而,目前尚无在体左心室心外膜起搏后复极离散的相关研究。方法 10只健康猪,应用电解剖标测系统(CARTO),在右心房(RA)、右心室(RV)心尖部心内膜(RVEndo)及左心室后壁心外膜(LVEpi)起搏下,分别标测左心室(LV)及右心室(RV)心内膜单相动作电位(MAP),测量不同部位起搏时的整体心室激动时间(AT)离散及整体心室复极结束时间(EOR)离散。结果平均每个心室标测121±35个点,RA起搏时EOR为63±12 ms,LVEndo起搏时EOR为94±17 ms,RVEndo起搏时EOR为72±18 ms;LVEpi起搏时EOR明显长于RA起搏时EOR(P<0.05),RVEndo起搏与RA起搏EOR没有差别(P>0.05)。结论 LVEpi起搏时整体心室肌复极离散较RA及RVEndo起搏时明显增加。  相似文献   

2.
目的评价整体心室复极离散度(d ispersion of ventricu lar repolarization,DVR)能否从心内膜几个邻近点或几个远距离点的标测来估测。方法应用CARTO标测系统,在10头猪左心室心内膜的(75±12)个位点记录单相动作电位。计算每一点复极结束时间(end-of-repolarization tim e,EORT)和动作电位时程(monophasic action potentialduration,MAPD)。关于EORT和MAPD的整体DVR与相应的局部DVR进行比较。局部DVR包括面积在2 cm2内的邻近DVR;还包括左室最早和最晚激动点间的远距离DVR1以及左室心尖部和外基底部间的远距离DVR2。结果关于EORT和MAPD的邻近DVR[(15±4)m s和(12±4)m s]显著小于相应的整体DVR[(84±31和77±26)m s,P<0.01]。远距离DVR1[(42±19和23±14)m s]和远距离DVR2[(25±16和18±11)m s]显著大于邻近DVR(P<0.01),但仍显著小于整体DVR(P<0.01)。结论从心内膜几个邻近点或几个远距离点的标测不能良好地估测整体DVR。在估测整体DVR中获取整体信息很重要。  相似文献   

3.
目的观察心脏不同部位起搏时体表心电图评价心室肌复极指标的变化,了解不同部位起搏对心室肌整体复极离散的影响。方法 10只健康猪,分别在右心房(RA)、右心室心尖部心内膜(RVEndo)及左心室心外膜(LVEpi)起搏,记录并测量体表心电图12个导联的T波峰-末间期(Tpe)和QT间期,计算Tpe平均值(Tpe-AVE)、Tpe最大值(Tpe-MAX)以及QT间期离散度(QTd),比较不同部位起搏时上述各参数的差异,进一步评价不同起部位对心室整体复极离散的影响。结果 LVEpi、RA、RVEndo起搏时的QT间期分别为(328±24)ms、(295±13)ms、(304±17)ms,LVEpi起搏时的QT间期明显长于RA及RVEndo起搏时的QT间期(P<0.05),RA与RVEndo起搏时QT间期没有明显差别。LVEpi、RA、RVEndo起搏的QT离散度(QTd)分别为(33±6)ms、(17±3)ms、(18±3)ms,LVEpi起搏时的QTd明显大于RA及RVEndo起搏时的QTd(P>0.05),RA与RVEndo起搏时QTd没有明显差别(P>0.05)。RA起搏时Tpe-AVE及Tpe-MAX分别为49±6ms及58±8 ms,与RVEndo起搏相近(49±8)ms及(60±8)ms,P>0.05);LVEpi起搏时Tpe-AVE及Tpe-MAX明显增大(63±7)ms及(71±8)ms,与RA、RVEndo起搏时比较两者(P<0.05)。结论与RA及RVEndo起搏时比较,LVEpi起搏时的QT间期、QTd、Tpe-AVE及Tpe-MAX均明显增大,LVEpi起搏可能会增加心室整体复极离散。  相似文献   

4.
心室肌的除极和复极具有一定顺序,在整体心脏上表现出异质性,复极离散度增加和某些室性心律失常的发生、发展密切相关[1-3]。临床上心内膜或心外膜单相动作电位(MAP)标测可较精确地反映心室肌复极不均一现象。1MAP标测的方法早在1959年,Hofman...  相似文献   

5.
目的:研究猪左心室心内膜整体复极顺序。方法:应用CARTO系统,在10只猪左心室心内膜的75±12个位点记录单相动作电位。计算每一点的局部激动时间(activation tim e,AT)、复极结束时间(end-of-repolarization tim e,EORT)和单相动作电位时程(monophasic action potential duration,MAPD),并且据此建立10套三维整体心室肌AT顺序、EORT顺序和MAPD长短顺序的标测图。结果:①EORT顺序图显示10只猪中有9只猪的EORT顺序明确地沿袭了激动顺序。②在最早的激动区域或附近记录到最长的MAPD,而在最晚的激动区域或附近则记录到最短的MAPD。③所有标测图的MAPD与AT成负线性相关,而EORT与AT成正线性相关。结论:猪左室心内膜存在复极梯度。激动顺序是复极顺序的一个决定因素。较晚的心室激动伴随着较短的MAPD,MAPD缩短幅度相对于局部激动的变晚程度,是决定复极方向和形态的关键因素。  相似文献   

6.
目的:探讨应用普通标测电极记录单相动作电位(MAP)的可行性,并对心房电生理特性做初步研究。方法:阵发性室上性心动过速行射频消融的患者12例,应用两根普通四极标测导管,于高位右房(HRA)和右房低位侧壁(LLW)两点顺序标测记录MAP。结果:共记录到21个满意的MAP信号,HRA处激动时间(AT)小于LLW处,动作电位时程(APD)和复极时间(RT)则相反(P0.05或P0.01),但S1S1刺激时的APD较窦律时缩短(P0.05),RT离散度明显小于APD离散度(均P0.01)。结论:无器质性心脏病者右房区域内存在复极离散。  相似文献   

7.
程序电刺激时心室复极离散度的研究   总被引:1,自引:0,他引:1  
了解程序电刺激 (PES)时心室复极离散度的变化 ,探讨PES诱发室性快速心律失常 (VTA)的可能机制。采用单相动作电位 (MAP)标测技术测定 10例无器质性心脏病的阵发性室上性心动过速患者接受PES时的心室复极离散度。结果 :S1 S1 刺激 ( 5 0 0ms)时的动作电位时程 (APD)的离散度 (APDd)与窦性心律时无明显差异 ( 34± 10msvs38± 9ms ,P >0 .0 5 )。随S1 S2 间期缩短 ,各标测点S2 的APD逐渐缩短 ,且与S1 S2 间期呈正相关 ,但激动时间 (AT)及其离散度 (ATd)、APDd、复极时间离散度 (RTd)逐渐延长 ;S1 S2 间期缩短至有效不应期 (ERP) +30ms后 ,S2 的APDd、RTd大于窦性心律及S1 S1 刺激时 (APDd :5 1± 8msvs 38± 9ms或 34± 10ms,P <0 .0 5 ;RTd :39± 10msvs2 4± 7ms,P<0 .0 5 ) ,但ATd无明显增大。心室内各点有效不应期离散度为 31± 14ms,ERP APD平均为 0 .89± 0 .0 8。认为在无器质性心脏病者PES可使心室复极离散度增大 ,但不增加传导差异 ,不易诱发VTA  相似文献   

8.
目的探讨心室复极离散度测定方法的可靠性.方法对19例无器质性心脏病者,应用左、右心室内膜单相动作电位(MAP)标测、腔内单极电图(UECG)和体表12导联同步心电图(ECG)3种方法研究心室复极离散度.结果UECG测值(UQ-Td,33±7ms)大于MAP测值(RTd,27±6ms,P<0.01),而小于体表心电图测值(Q-Td,38±7m,P<0.01),即Q-Td>UQ-Td>R-Td,但UQ-Td与R-Td、UQ-Td与Q-Td、R-Td与Q-Td均呈显著线性相关(r=0.75、0.87,0.78,P均<0.01).结论体表心电图Q-Td可以代表心室复极离散.  相似文献   

9.
阵发性心房颤动患者心房复极离散度的研究   总被引:3,自引:0,他引:3  
目的 通过记录阵发性心房颤动 (房颤 )患者心房单相动作电位 (MAP) ,分析心房复极离散度与房颤发生的关系。方法 特发性阵发性房颤患者与无自发房颤病史的阵发性室上性心动过速患者各 1 5例 ,均接受心内电生理检查和 /或导管射频消融治疗。两根 MAP电极于右心房共取 4~ 1 0个不同部位进行同步的窦性心律基础刺激 (S1)及期前刺激 S2 时的 MAP记录。测量、计算心房复极离散度(RTd)及动作电位时限和局部冲动时间的离散度 (APDd、ATd)。 结果 窦性心律时房颤组最大 RTd显著大于对照组 (1 2 3 .69± 54.67) ms比 (64 .2 5± 2 3 .2 9) ms,(P<0 .0 1 )。其差异主要来源于 APDd(1 1 5.0 0± 4 6.90 ) ms比 (57.56± 3 3 .57) ms,(P<0 .0 1 ) ,ATd差异无显著性。随 S1、S2 的加入 ,各组局部激动时间和离散度逐渐增大 ,而动作电位时限逐渐缩短 ,且房颤组的这种改变程度显著大于对照组。在S1时无房颤发生 ,加入期前刺激时 ,大多数房颤组患者均多次诱发出短阵房颤。其诱发率及次数均显著高于对照组。 结论 研究结果表明 ,MAP记录技术是临床观察、分析心房复极离散度及其在阵发性房颤中的作用的较佳方法。心房复极离散度的增加是阵发性房颤发生的重要因素。期前刺激时动作电位时限的缩短和离散以及传导障碍在  相似文献   

10.
目的 应用单相动用电位(MAP)技术,系统研究T民击引起的复极离工用(SIDR)与诱发心室颤动(VF)的关系。方法 截尾指数为65%/65%,脉宽5ms的缀相电流,以电击强度与配对间期的随机组合施加于稳态起r Langendorff离体灌流家兔心脏的舒张期。8个心外膜和2个心内膜位点同步记录MAP。SIDR定义为MAP同起记录中最长与最短电击后复极时间之差。结果 诱发VF的电击引起的SIDR为(6  相似文献   

11.
The aim of this study was to evaluate whether the QT dispersion measured from 12-lead electrocardiogram (ECG) can estimate the global dispersion of ventricular repolarization (DVR) measured using a monophasic action potential (MAP) mapping technique. Monophasic action potentials were recorded from 75 +/- 12 left ventricular sites in 10 pigs and from 48 +/- 16 left or right ventricular sites in 15 patients using the CARTO mapping system. The maximum DVRs in both end-of-repolarization and MAP duration among all the mapped sites were calculated and termed as global DVR for each measurement. QT intervals, QT peak and QT end , were measured from the 12-lead ECG, and QT dispersions; namely the differences between the maximum and the minimum of the QT peak and QT end were calculated. We found that QT dispersions were significantly smaller than (P < .05) and poorly correlated with the global DVRs both in pigs and patients. Bland-Altman agreement analysis demonstrated a marked variation of the differences and an obvious lack of agreement between the results obtained using the ECG and the MAP methods. In our patients, the global DVR increased markedly during ventricular tachycardia as compared with that during sinus rhythm (P < .05), whereas there was no significant difference in QT dispersion between these 2 subgroups. In conclusion, QT dispersion on the surface ECG could not estimate the global DVR measured using the MAP mapping technique. These findings are not consistent with some previously reported observations, suggesting the need for reappraisal of the electrophysiological implications of QT dispersion.  相似文献   

12.
INTRODUCTION: Activation recovery time (ART), defined as the time from the earliest ventricular activation time to the end of T wave on unipolar electrograms, has been used as an index of myocardial repolarization time. However, it is unknown whether the ART can be used to estimate the global sequence and dispersion of ventricular repolarization as determined by the monophasic action potential (MAP) mapping technique. METHODS AND RESULTS: Endocardial MAPs and unipolar electrograms were simultaneously recorded using the CARTO system from 34 +/- 12 left (n = 6) or right (n = 9) ventricular sites in 12 patients. End-of-repolarization (EOR) times from the MAPs and ARTs from the unipolar electrograms were calculated, based on which 15 sets of 3-dimensional maps of global EOR sequence and ART sequence were reconstructed. The ART sequence was consistent with the EOR sequence in 14 of 15 maps. In the 473 paired measurements obtained, the differences between the ART and the EOR time were 2 +/- 22 milliseconds (NS). A significant positive correlation between the ART and the EOR time was found in all the maps (r = 0.58 +/- 0.22). Agreement analyses showed that the differences between these 2 measurements were almost all within the range of mean difference +/- 2 SD for each individual map and for all the 473 recordings. The global dispersion of ART was 79 +/- 35 milliseconds, as compared with that of EOR time of 78 +/- 35 milliseconds (NS). CONCLUSION: The ART from unipolar electrograms is a good estimate of EOR time measured from MAPs, suggesting the usefulness of the former in evaluation of global sequence and dispersion of ventricular repolarization.  相似文献   

13.
AIMS: To evaluate the usefulness of the signed value of monophasicaction potential duration difference in analysing the causeof dispersion of ventricular repolarization. METHODS AND RESULTS: Monophasic action potentials were simultaneously recorded fromthe right ventricular apex and outflow tract during programmedstimulation in 36 patients with ventricular arrhythmias. Thetime difference between the ends of repolarization on the twomonophasic action potentials was used as a measure of the dispersionof ventricular repolarization, and the signed value of the monophasicaction potential duration difference was used to specify thecontributions of the activation time difference and the monophasicaction potential duration difference to the dispersion of ventricularrepolarization. During right ventricular pacing, single anddouble programmed stimulation and at the induction of ventriculararrhythmias, the dispersion of ventricular repolarization andthe signed value of monophasic action potential duration differencewere markedly greater in the 11 patients with polymorphic ventriculartachycardia/ventricular fibrillation induced than in the 13patients with monomorphic ventricular tachycardia induced, andin the 10 patients with clinical polymorphic ventricular tachycardia/ventricularfibrillation/cardiac arrest than in the 12 patients with sustainedmonomorphic ventricular tachycardia. This disclosed that theincreased dispersion of ventricular repolarization was causedby increases in both the activation time difference and themonophasic action potential duration difference in the former,but mainly by an increased activation time difference in thelatter groups. CONCLUSION: The signed value of monophasic action potential duration differencecan specify whether an increased dispersion of ventricular repolarizationis caused by in-homogeneous repolarization, inhomogeneous conductionor both, and thereby it is useful in study of the mechanismof ventricular arrhythmias.  相似文献   

14.
Summary The present study was designed to combine the monophasic action potential (MAP) recording technique with a well-established canine isolated, bloodperfused ventricular septum preparation for examining, simultaneously, electrical and mechanical drug-induced changes. A MAP catheter was positioned onto the base of a papillary muscle for recording the local MAP, using a manual micromanipulator together with a commercially available catheter sheath to keep the optimal contact pressure against the ventricular wall. The catheter sheath was filled with saline to eliminate the background electrical noise. Tetrodotoxin, disopyramide, lidocaine, and verapamil were used to clarify the potential utility of the preparation. Tetrodotoxin and lidocaine shortened the MAP duration, while disopyramide prolonged it. Verapamil slightly shortened the MAP duration but not significantly. Each drug showed negative inotropic and coronary vasodilator effects. Sodium channel blockers slowed intraventricular conduction and decreased the maximum upstroke velocity of MAP, while verapamil showed no effects. These results suggest that utilization of the bloodperfused ventricular septum preparation together with MAP recording will become a valuable model for evaluating drugs with multiple sites of action on cardiac muscles.This study was supported in part by a Grant-in-Aid for Scientific Research (08770064) from the Japanese Ministry of Education, Science and Culture.  相似文献   

15.
目的 观察索他洛尔对兔在体心脏左心室壁各层心肌复极的影响 ,以证实在体心肌 M细胞的存在 ,探讨其与心律失常的关系。 方法 采用单相动作电位 (m onophasic action potential,MAP)记录技术 ,同步记录 12只开胸兔左心室外膜心肌 (epicardium ,Epi)、中层心肌 (m id- myocardium ,Mid)和心内膜心肌 (endocardium ,Endo)的 MAP,静脉注射索他洛尔后 ,测量 3层心肌 MAP的复极时限和跨心室壁心肌复极离散度 (transm ural dispersion of repolarization,TDR)。 结果  1用药前 Epi、Mid、Endo的 MAP10 0 %复极时限 (APD1 0 0 )分别为 (136± 16 )、(15 2± 19)、(15 0± 2 0 ) m s,TDR为 (17± 8) m s。每间隔 30 m in静脉注射索他洛尔 0 .5、1.0、1.5和 2 .0 m g· kg- 1后发现 ,索他洛尔剂量依赖性延长 3层心肌的 APD1 0 0 ,其中以延长 Mid的 APD1 0 0 更为明显 ,对 Epi和 Endo的 APD1 0 0 延长程度相近 ,使 TDR增加 ;至静脉注射 2 .0 mg· kg- 1 后 ,Epi、Mid、Endo的 APD1 0 0 分别为 (177± 30 )、(2 34± 32 )、(194± 30 ) ms,TDR为 (5 7± 15 ) ms(P <0 .0 5 ) ;2索他洛尔剂量依赖性地增加尖端扭转性室性心动过速 (torsade depointes,TDP)的发生率。 结论 在体兔心肌存在 M细胞。索他洛尔增加兔  相似文献   

16.
急性缺血对犬在体心肌跨心室壁复极不均一性的影响   总被引:7,自引:0,他引:7  
目的:探讨急性缺血对犬在体心肌跨心室壁复极不均一性及与心律失常的关系。方法:健康家犬10只,应用单相动作电位记录技术,同步记录健康家犬在体阻断左前降支主干前后心外膜、中层及心内膜心肌单相动作电位及体表心电图,分析相关参数的变化。结果:3层心肌单相动作电位时程正常供血状态下差异无显著性意义(P>0.05),急性缺血状态下则均明显缩短,且心外膜、心内膜的缩短程度较中层心肌更为明显,差异有显著性意义(P<0.05)。3层心肌间跨室壁复极离散度增大。10只犬中正常供血状态下无一例出现心律失常,急性缺血30min内4只出现了室性心动过速或心室颤动死亡,恶性心律失常发生率达40%。结论:急性缺血时犬在体心肌跨心室壁复极离散度增大,可能是导致缺血性室性心律失常的原因之一。  相似文献   

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