慢性压力超负荷对兔左室跨壁单相动作电位的影响

研究慢性压力超负荷对兔左室跨壁单相动作电位(MAP)的影响。24只兔随机分为压力超负荷组和假手术组。压力超负荷组用开胸缩窄升主动脉的方法建立心室压力超负荷动物模型,假手术组仅行开胸术。5个月后对所有动物行在体电生理检查,在基础状态和给予短阵快速刺激后分别测量左室游离壁三层心肌MAP时程(MAPD)和有效不应期(ERP),并计算MAPD的跨壁离散度(TD)。结果:基础状态下,压力超负荷组兔左室前壁三层心肌复极90%和50%的MAPD(MAPD90、MAPD50)较假手术组明显缩短,而MAPD90250和TD没有明显变化,ERP缩短,TD90无明显变化。在左室外膜给予数次短阵快速刺激以后,压力超负荷组三层心室肌MAPD90进一步缩短,MAPD90250也明显缩短,TD明显增加,而MAPD50没有明显变化。MAPD90250的变化导致MAPD90的跨壁梯度发生重排,而假手术组MAPD90及其分布没有明显变化,两组ERP在短阵快速刺激以后无明显变化。结论:慢性心室压力超负荷引起心室肥厚和跨壁MAP分布的明显变化,可能为室性心律失常发生的基质。     

猪整体和局部心室复极离散度的单相动作电位标测比较

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。     

单相动作电位技术检测心房复极的电生理特点

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。     

应用单相动作电位技术研究心室肌复极离散度

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...     

使用铂电极记录单相动作电位的可行性研究

目的探讨使用用于射频消融的普通铂电极记录心内膜单相动作电位(MAP)的可行性。方法 20例阵发性室上性心动过速行导管消融的患者分两组,分别使用铂电极和银-氯化银(Ag-AgCl)电极在右室心尖部及右室流出道进行MAP标测,测量各标测点MAP的振幅(AMP)、动作电位复极达90%的时程(APD90)、激动时间(AT)和复极时间(RT),比较两组间各指标的差异。结果在右室心尖部和右室流出道Ag-AgCl电极组和铂电极组分别测得48和46个标测点,其中铂电极组仅有3个标测点基线干扰较大,并且该组振幅大于10 mV的标测点共有33个,基本满足稳定的MAP信号的要求。与Ag-AgCl电极组相比,铂电极组测得的MAP的AMP、APD90、AT、RT值均没有显著差异(P均0.05)。结论在临床研究中使用铂电极代替Ag-AgCl接触电极作为同时记录MAP和射频消融的两用电极具有可行性。     

通过单相动作电位评价不同部位起搏时猪整体心脏复极离散变化

目的 通过对猪心脏不同部位起搏,观察不同激动顺序对整体心脏复极离散的影响.方法 10只健康猪,应用电解剖标测系统（Carto系统）,在右心房（RA）、右心室心尖部心内膜（RVEndo）及左心室后壁心外膜（ LVEpi）起搏,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,LVEpi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差异无统计学意义（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.     

猪左心室内膜整体复极顺序的单相动作电位标测

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。     

跨室壁复极离散度变化对心电图T波形态影响的电生理研究

目的 :探讨在体情况下心肌跨室壁复极离散度 （TDR）变化对心电图 T波影响的可能机制。方法 :运用单相动作电位 （MAP）记录技术 ,同步记录 14只开胸兔的左室心肌心外膜层 （Epi） ,中层 （Mid） ,内膜层 （Endo）的 MAP,分别予以静脉注射索他洛尔 （dl- sotalol） ,海葵毒素 （ATX- II）后 ,观察跨室壁复极离散的变化及同时心电图 T波的相应改变。结果 :1dl- sotalol导致 Mid层细胞 MAP的复极时间 （RT）显著的延长 （从 2 0 2± 19m s到 395± 34ms） ,TDR增大 （从 11± 4 m s到 75± 2 5 ms） ,QT间期延长 （从 2 0 8± 16 ms到 397± 33m s） ,3层心肌 MAP的 3相复极不同程度的延长 ,使复极电位梯度变化 ,产生增宽、低幅有切迹的 T波。 2 ATX- II导致 Mid层细胞 MAP的 RT显著的延长 （从 370± 34m s到 4 73± 35 m s） ,TDR增大 （从 4 0± 2 1ms到 6 2± 19m s） ,QT间期延长 （从 372± 33ms到 4 79± 33ms） ,3层心肌 MAP的 2相平台期不同程度延长 ,使复极电位梯度变化 ,产生晚现 T波 ,波幅增大。结论 :在体兔心肌跨壁复极离散度的变化对心电图 T波的形态有重要影响     

体表心电图、腔内单极电图与单相动作电位测定心室复极离散度相关分析

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.     

Dispersion of repolarization following double and triple programmed stimulation: A clinical study using the monophasic action potential recording technique

To study the dispersion of ventricular repolarization followingdouble and triple programmed stimulation and its correlationwith the inducibility of ventricular arrhythmias, monophasicaction potentials were simultaneously recorded from the rightventricular apex and outflow tract during programmed stimulationin 12 patients with ventricular arrhythmias and a normal QTinterval. The time difference between the ends of the two monophasicaction potentials were used as a measure of the dispersion ofventricular repolarization, which consists of the activationtime difference and the monophasic action potential durationdifference. During double and triple programmed stimulation, the dispersionof ventricular repolarization increased significantly with theshortening of the coupling interval but decreased slightly withthe shortening of the coupling interval but decreased slightlywith the shortening of the preceding interval. The inductionof the ventricular arrhythmias in these patients was invariablyassociated with a marked increase in the dispersion of ventricularrepolarization. The maximal dispersion of ventricular repolarizationwas significantly larger in the seven patients with polymorphicventricular tachycardia and/or ventricular flutter/fibrillationinduced than in the four patients with monomorphic ventriculartachycardia induced. Analysis of the two components of the dispersionof ventricular repolarization revealed that the increased dispersionof ventricular repolarization was mainly caused by an increasein the activation time difference in the monomorphic ventriculartachycardia subgroup, and by increases in both the activationtime difference and monophasic action potential duration differencein the polymorphic ventricular tachycardia/fibrillation subgroup. These findings suggest that increased dispersion of ventricularrepolarization is one of the underlying mechanisms accountingfor the myocardial vulnerability to ventricular arrhythmiasand that repolarization disturbance is important for the genesisof polymorphic ventricular tachycardia/fibrillation.     

In vitro validation of a new cardiac catheter technique for recording monophasic action potentials

Monophasic action potential (MAP) recording with non-suction, 'contact' electrode catheters has been shown possible and safe during clinical catheterization, but direct validation of this new technique is lacking. We therefore recorded these contact electrode MAPs simultaneously with transmembrane action potentials (TAPs) from closely adjacent sites in perfused and superfused rabbit septum preparations and performed a quantitative comparison between the two signals for duration and area at 30, 60 and 90% repolarization. To obtain a variety of action potential durations and configurations for the comparison, the rate and rhythm of stimulation and the extracellular calcium or potassium ion concentration were changed. With action potential duration at 90% repolarization made to vary from 150 to 513 ms, the mean absolute difference +/- SD between the simultaneous intra- and extracellular recordings was 5.4 +/- 11.3 ms and the linear correlation coefficient was r = 0.96 +/- 0.03. Similar agreement between the two types of recordings was found for measurements for area and at 60 and 30% repolarization levels. These data confirm that MAPs recorded with this clinically safe contact electrode technique can be used to measure accurately the repolarization time course of transmembrane action potentials.     

粉防己碱对家犬在体心脏单相动作电位的影响

目的:研究粉防己碱(Tet)对家犬在体心室肌单相动作电位(MAP)和有效不应期(ERP)的影响,探讨其抗心律失常的可能机制。方法:家犬14只,随机分为Tet组和维拉帕米(Ver)组,记录右室心内膜MAP及心电图Ⅱ导联,比较不同剂量的Tet和Ver对MAP振幅(MAPA)、复极化达50％和90％一点到MAP上升支的水平距离(MAPD50、MAPD90)、ERP及ERP/MAPD90。结果:Tet引起窦性心率减慢,随剂量增加(3～12 mg/kg)ERP延长、ERP/MAPD90增大,但对MAPA、MAPD50、MAPD90无明显影响;而Ver除延长ERP,增大ERP/MAPD90,还缩短MAPD50、MAPD90。结论:Tet对MAP的影响可能除钙拮抗作用外,还有别的离子基础;延长ERP、增大ERP/MAPD90可能是其抗心律失常的机制。     

Effects of antiarrhythmic drugs on the monophasic action potential of the canine isolated, blood-perfused ventricular septum preparation

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.     

Signed value of monophasic action potential duration difference: A useful measure in evaluation of dispersion of repolarization in patients with ventricular arrhythmias

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.     

急性缺血时犬3层心肌单向动作电位时程和有效不应期变化

目的:探讨急性缺血对犬在体3层心肌的电生理影响。方法:将12只犬随机分为急性缺血组(6只)和假手术组(6只)。应用单向动作电位(MAP)技术和特制的复合电极同步记录MAP和测定有效不应期(ERP),并分析跨室壁复极离散(TDR)和跨室壁不应期离散(TDE)。结果:在急性缺血组,MAP时程从[(201·67±21·42)ms缩短至(169·50±13·81)ms,P<0·05],而ERP不同程度地延长,且TDE增大。在假手术组,MAP时程和ERP没有明显变化。2组3层心肌之间MAP时程是一致的,不存在TDR。结论:急性缺血时MAP时程缩短,但3层心肌之间没有差别,而ERP延长伴随TDE增大。这可能在急性缺血时心律失常的发生中扮演重要角色。     

不同起搏部位对正常犬和长QT间期犬模型在体跨心室壁复极离散的影响

目的以正常犬和长QT间期(LQT)犬模型的在体3层心肌单向动作电位时限(MAPD)和跨室壁复极离散(TDR)、体表心电图上QT间期和Tp-Te间期等为指标,研究不同部位起搏,尤其是左心室外膜参与起搏后心肌复极特性的变化.通过这种模拟临床上心室再同步治疗的方法,旨在观察左心室起搏、双心室起搏是否会增加恶性室性心律失常发生的危险性.方法 8只健康成年犬经导管射频消融希氏束制备三度房室阻滞模型.开胸手术后分别在左心室外膜、右心室内膜和双心室起搏时同步记录体表心电图和心内膜下、中层、心外膜下3层心肌的单相动作电位(MAP),测定QT间期、Tp-Te间期和3层心肌的MAPD、TDR.然后以氯化铯(CsCl)制备LQT犬模型并重复上述实验.结果在正常犬,左心室外膜与双心室起搏后,心内膜下、中层、心外膜下3层心肌的MAPD均有延长,并有TDR的增大(左心室外膜起搏47.16 ms、双心室起搏37.54 ms、右心室内膜起搏26.75 ms,P＜0.001),体表心电图Tp-Te间期的变化与之平行.在LQT犬,在CsCl使3层心肌MAPD延长的基础上,左心室外膜参与起搏进一步明显增大TDR,而CsCl增大TDR的作用被掩盖.结论左心室心外膜与双心室起搏后使心内膜下、中层、心外膜下3层心肌的MAPD均延长并使TDR增大,可能成为导致恶性室性心律失常的基础.在临床上推广应用心室再同步技术治疗充血性心力衰竭患者时,这一问题必须引起高度重视.     

缬沙坦对兔在体肥厚心肌跨室壁复极不均一性的影响

目的:探讨兔在体左心室肥厚心肌跨室壁复极不均一性的变化及缬沙坦的影响。方法:30只兔均分为3组,分别为肥厚组(以腹主动脉缩窄术制备心肌肥厚模型);治疗组(腹主动脉缩窄术后给予缬沙坦口服);对照组(仅分离腹主动脉而不予缩窄)。采用自制复合式电极在兔左心室前壁同步记录心内膜、心肌中层、心外膜在体三层心肌单相动作电位(MAP)。结果:肥厚组平均动脉压、心脏重量及其与体重比率、左心室游离壁厚度均显著大于治疗组和对照组。肥厚组3层心肌单相动作电位时程(MAPD100)(内膜:191±19 ms,中层:244±24 ms,外膜:196±15ms)较对照组(内膜:170±18 ms,中层:172±15 ms,外膜:168±16 ms)均显著延长(中层P<0.01,内膜、外膜P<0.05,n=10),且以中层心肌MAPD100延长最为明显。而治疗组与对照组3层心肌MAPD100比较均无明显差异。结论:缬沙坦可阻止兔在体左心室肥厚心肌跨室壁复极不均一性的增大。