急性心肌缺血时肥厚左心室跨壁复极离散度及心律失常发生机制

目的:探讨急性心肌缺血过程中肥厚左心室跨壁复极离散度变化及与室性心律失常关系。方法:分别记录肥厚及正常对照心室肌标本在模拟缺血过程中、不同刺激周长下内外膜动作电位及跨壁复极离散度变化;对比室性心律失常发生率、分析机制。结果:①和对照组相比,肥厚组在缺血各个时段跨壁复极离散度均显著升高,且随缺血时间、刺激周长的延长逐步递增。②肥厚组在缺血过程中早后除极、延迟后除极发生率显著高于对照组,且多次形成跨壁折返性心律失常。对照组虽有延迟后除极,但未能形成跨壁折返。结论:肥厚心室跨壁复极离散度存在缺血时间、刺激周长的双重依赖;在此基础上早后除极、延迟后除极诱发跨壁折返是缺血肥厚心室心律失常的主要机制之一。     

兔肥厚左心室跨壁复极离散度和室性心律失常发生机制

目的 探讨肥厚左心室跨壁复极离散度变化及室性心律失常发生机制.方法 制作压力超负荷兔模型,分别记录对照组、肥厚组心室肌内、外膜动作电位并同步记录跨室壁心电图,比较两组动作电位时限（APD90）、跨心室壁复极离散度（TDR）和室性心律失常发生率、尖端扭转性室性心动过速（Tdp）危险度评分.结果 （1）与对照组相比,肥厚组内、外膜APD90显著延长,以内膜层心肌更为明显;TDR显著增大（P＜0.01）;上述变化呈现显著慢频率依赖性;（2）肥厚组室性心律失常发生率、Tdp危险度评分明显高于对照组.结论 动作电位时限延长、跨心室壁复极离散度增大基础上的早期后除极和跨室壁折返激动是肥厚心室心律失常的主要机制.     

QT dispersion does not represent electrocardiographic interlead heterogeneity of ventricular repolarization

INTRODUCTION: QT dispersion (QTd, range of QT intervals in 12 ECG leads) is thought to reflect spatial heterogeneity of ventricular refractoriness. However, QTd may be largely due to projections of the repolarization dipole rather than "nondipolar" signals. METHODS AND RESULTS: Seventy-eight normal subjects (47+/-16 years, 23 women), 68 hypertrophic cardiomyopathy patients (HCM; 38+/-15 years, 21 women), 72 dilated cardiomyopathy patients (DCM; 48+/-15 years, 29 women), and 81 survivors of acute myocardial infarction (AMI; 63+/-12 years, 20 women) had digital 12-lead resting supine ECGs recorded (10 ECGs recorded in each subject and results averaged). In each ECG lead, QT interval was measured under operator review by QT Guard (GE Marquette) to obtain QTd. QTd was expressed as the range, standard deviation, and highest-to-lowest quartile difference of QT interval in all measurable leads. Singular value decomposition transferred ECGs into a minimum dimensional time orthogonal space. The first three components represented the ECG dipole; other components represented nondipolar signals. The power of the T wave nondipolar within the total components was computed to measure spatial repolarization heterogeneity (relative T wave residuum, TWR). QTd was 33.6+/-18.3, 47.0+/-19.3, 34.8+/-21.2, and 57.5+/-25.3 msec in normals, HCM, DCM, and AMI, respectively (normals vs DCM: NS, other P < 0.009). TWR was 0.029%+/-0.031%, 0.067%+/-0.067%, 0.112%+/-0.154%, and 0.186%+/-0.308% in normals, HCM, DCM, and AMI (HCM vs DCM: NS, other P < 0.006). The correlations between QTd and TWR were r = -0.0446, 0.2805, -0.1531, and 0.0771 (P = 0.03 for HCM, other NS) in normals, HCM, DCM, and AMI, respectively. CONCLUSION: Spatial heterogeneity of ventricular repolarization exists and is measurable in 12-lead resting ECGs. It differs between different clinical groups, but the so-called QT dispersion is unrelated to it.     

Increased dispersion of ventricular repolarization and ventricular tachyarrhythmias in the globally ischaemic rabbit heart

Contemporary concepts of ischaemic ventricular tachyarrhythmias(VTA) are based on increased electrophysiological heterogeneityof the myocardium. We developed a multi-site monophasic actionpotential recording system for an isolated rabbit heart to studythe effects of global ischaemia on the electrophysiologicalproperties at different ventricular sites simultaneously. Thehearts were paced from the right ventricle (RV) andconductiontime (CT), action potential duration (APD) and total repolarizationtime (TRT= [CT + APD]) were measured during normal perfusionand ischaemia. The dispersion of these parameters was calculatedas the maximal difference between simultaneous recordings. Inducibilityof VTA by programmed extrastimulation (ES) was investigatedunder normal and ischaemic conditions. During global ischaemia, CT increased progressivey showing afaster and greater increase at the left ventricle (LV) thanat the RV. After 10 min the prolongation of CT reached a plateauat the LV while it continued to rise in the RV. The dispersionof CT increased from 14 ± 2.7 ms during normal perfusionto a maximum of 79.8 ± 17.2 ms after 14 min of ischaemnia(P<00001). APD was uniform at the three sites (190.9±02,185.0 and 179.3±9.8 ms, ns) during normal perfusion butchanged non-uniformly during ischaemia. There was a transientlengthening of APD until 1 and 3 min of ischaemia at the LVsites followed by a rapid shortening of APD. At the RV site,APD continued to increase until 5 min of ischaemia and thenshortened gradually. Consequently, dispersion of APD showeda rapid initial rise from 177.8 ± 2.7 ms to 77.8 ±10 ms (P<0.0001) followed by a slower final increase. TRTwas uniform during normal perfusion (210.4 ± 10.3, 213.1±7.8,212.1±10.3 ms, ns) but became non-uniform during globalischaemia. The dispersion of TRT increased from 15.4±4.2ms to 92.6 ± 23.2 ms (P<0.0001) during 14 min of globalischaemia. Both CT and APD contributed independently to TRTand could either augment or partially compensate for the ischaemicalterations of the other parameter. ES induced VTA only during ischaemia (3.7±1.1 VTA perheart, P<0.0001) at coupling intervals between 220 and 380ms. The dispersion of TRT of the last regular beat precedingVTA was 67.7±17.4 ms (P<0.001). ES which triggeredVTA showed a more than two-fold increase of CT dispersion comparedto the last steady state beat (122.7±29.4%, P = 0.0001). The present results show that global ischaemia results in considerableelectrophysiologic heterogeneity in the intact heart. Thesechanges may be regarded as a suitable basis of VTA, inducedby ES.     

Increased dispersion of ventricular repolarization and ventricular tachyarrhythmias in the globally ischaemic rabbit heart

Contemporary concepts of ischaemic ventricular tachyarrhythmias(VTA) are based on increased electrophysiological heterogeneityof the myocardium. We developed a multi-site monophasic actionpotential recording system for an isolated rabbit heart to studythe effects of global ischaemia on the electrophysiologicalproperties at different ventricular sites simultaneously. Thehearts were paced from the right ventricle (RV) andconductiontime (CT), action potential duration (APD) and total repolarizationtime (TRT= [CT + APD]) were measured during normal perfusionand ischaemia. The dispersion of these parameters was calculatedas the maximal difference between simultaneous recordings. Inducibilityof VTA by programmed extrastimulation (ES) was investigatedunder normal and ischaemic conditions. During global ischaemia, CT increased progressivey showing afaster and greater increase at the left ventricle (LV) thanat the RV. After 10 min the prolongation of CT reached a plateauat the LV while it continued to rise in the RV. The dispersionof CT increased from 14 ± 2.7 ms during normal perfusionto a maximum of 79.8 ± 17.2 ms after 14 min of ischaemnia(P<00001). APD was uniform at the three sites (190.9±02,185.0 and 179.3±9.8 ms, ns) during normal perfusion butchanged non-uniformly during ischaemia. There was a transientlengthening of APD until 1 and 3 min of ischaemia at the LVsites followed by a rapid shortening of APD. At the RV site,APD continued to increase until 5 min of ischaemia and thenshortened gradually. Consequently, dispersion of APD showeda rapid initial rise from 177.8 ± 2.7 ms to 77.8 ±10 ms (P<0.0001) followed by a slower final increase. TRTwas uniform during normal perfusion (210.4 ± 10.3, 213.1±7.8,212.1±10.3 ms, ns) but became non-uniform during globalischaemia. The dispersion of TRT increased from 15.4±4.2ms to 92.6 ± 23.2 ms (P<0.0001) during 14 min of globalischaemia. Both CT and APD contributed independently to TRTand could either augment or partially compensate for the ischaemicalterations of the other parameter. ES induced VTA only during ischaemia (3.7±1.1 VTA perheart, P<0.0001) at coupling intervals between 220 and 380ms. The dispersion of TRT of the last regular beat precedingVTA was 67.7±17.4 ms (P<0.001). ES which triggeredVTA showed a more than two-fold increase of CT dispersion comparedto the last steady state beat (122.7±29.4%, P = 0.0001). The present results show that global ischaemia results in considerableelectrophysiologic heterogeneity in the intact heart. Thesechanges may be regarded as a suitable basis of VTA, inducedby ES.     

卡维地洛对慢性压力超负荷兔左心室跨壁复极离散度的影响

目的探讨卡维地洛长期干预对慢性压力超负荷兔左心室跨壁复极离散度的影响。方法慢性压力超负荷兔模型随机分为结扎组和卡维地洛干预组（CVD组）；分别记录两组左心室心肌内、外膜动作电位并同步记录跨壁心电图，比较两组动作电位时限（APD90）、跨心室壁复极离散度（TDR）、室性心律失常发生率、超声心动图指标和左心室质量与体重比值。结果（1）CVD组左心室射血分数高于结扎组（P〈0．05），左心室质量与体重比值低于结扎组（P〈0．01），差异均有统计学意义。（2）CVD组左心室内、外膜APD90、TDR、QT间期、心律失常发生率较结扎组降低（P〈0．05）。结论卡维地洛长期干预能有效改善肥厚左心室结构和收缩功能；能显著降低动作电位时限、跨壁复极离散度和室性心律失常发生率，改善肥厚左心室结构重构和电重构。     

左心室M层起搏对犬跨室壁复极离散的影响

目的 研究心室M层起搏对犬跨室壁复极离散(TDR)的影响,探讨采用心室M层起搏技术防治跨室壁复极离散增大相关性心律失常的可行性.方法 制作犬左心室楔形心肌组织块模型,观察心内、外膜及M层起搏时,各层心肌动作电位时限(APD)及TDR的变化.结果 分别行心室肌内、外膜和M层起搏,心肌各层APD差异无统计学意义(P＞0.05)；但M层起搏时,TDR较外膜起搏明显减小[(34.9±5.4)ns对(71.5±6.1)ms,P＜0.01]；与内膜起搏相比差异无统计学意义[(34.9±5.4)ms对(35.9±5.4)ms,P＞0.05].结论 与心外膜起搏相比,M层起搏可有效减小TDR；但与心内膜起搏相比,差异无统计学意义.     

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     

Shock-Induced Dispersion of Ventricular Repolarization:

Shock-induced Dispersion and VF Induction. Introduction: Shock-induced dispersion of ventricular repolarization (SIDR) caused by an electrical field stimulus has been suggested as a mechanism of ventricular fibrillation (VF) induction: however, this hypothesis has not been studied systematically in the intact heart. Likewise, the mechanism underlying the upper (ULV) and lower (LLV) limit of vulnerability remains unclear.
Methods and Results: In eight Langendorff-perfused rabbit hearts, monophasic action potentials were recorded simultaneously from ten different sites of both ventricles. Truncated biphasic T wave shocks were randomly delivered at various coupling intervals and strengths, exceeding the vulnerable window, ULV, and LLV. SIDR, defined as the difference between the longest and shortest postshock repolarization times, was 64 ± 15 msec for sbocks inducing VF. SIDR was 41 ± 17 msec for shocks delivered above the ULV, and 33 ± 14 and 27 ± 8 msec for shocks delivered 10 msec before and after the vulnerable window, respectively (all P < 0.01 vs VF-inducing shocks). Although SIDR was larger for shocks delivered below the LLV(93 ± 24 msec, P < 0.01 vs VF-inducing shocks), the repolarization extension was significantly smaller for shocks below the LLV (10.3%± 3.9% vs 16.3%± 4.9%, P < 0.01).
Conclusion: SIDR is influenced by the shock timing and intensity. Large SIDR within the vulnerable window and an SIDR decrease toward its borders suggest that SIDR is essential for VF induction. The decrease in SIDR toward greater shock strengths may explain the ULV. Small repolarization extension for shocks below the LLV may explain why these shocks, despite producing large SIDR, fail to induce VF.     

四氢巴马汀对在体犬跨室壁复极离散度的影响

从跨室壁复极离散度(TDR)的角度研究左旋四氢巴马汀(L-THP)的电生理作用。采用自制电极同步记录在体犬左室三层心肌细胞的单向动作电位(MAP),观察静脉注射L-THP前后动作电位时程(APD)、振幅(APA)、TDR及各层心肌有效不应期(ERP)的变化。结果:应用L-THP后三层心肌的动作电位复极90%的时程均延长(内、中、外层心肌分别为189.67±23.29msvs182.83±23.70ms、194.67±24.12msvs192.17±24.49ms和185.08±24.53msvs173.42±22.06ms,P均<0.01),内、外层心肌ERP显著增加(分别为164.54±20.53msvs159.08±20.08ms、161.60±21.28msvs150.99±18.93ms,P<0.01)、TDR降低(9.58±2.94msvs18.75±3.77ms,P<0.01),对APA无明显影响。结论:L-THP降低心室肌的TDR,延长心室内、外膜心肌细胞的ERP。     

右室心尖部和间隔部S1S2刺激电重构后对跨室壁复极离散的影响

目的通过观察右室不同部位S1S2刺激电重构后对室壁QRS间期、QRS波起始至T波顶点间期（QTp）、QT间期和T波峰末间期（Tp2e）影响,分析不同部位起搏对跨室壁复极离散的影响。方法选取因阵发性室上性心动过速拟行射频消融患者18例,随机分心尖部刺激组（RVA组,n=9）和间隔部刺激组（RVS组,n=9）,分别行S1S2刺激,测量每组体表起搏心电图V1导联S2刺激的QRS间期、QRS波起始至T波顶点间期（QTp）、QT间期和T波峰末间期（Tp2e）并进行统计分析。结果 RVS组较RVA组的QRS间期、QTp无差异、至S1S2500/260ms后QT间期及Tp2e明显减低;两组均随S1S2刺激间期缩短QT间期及Tp2e明显增大,而QRS间期及QTp无差异。结论电重构后RVS组比RVA组心室跨壁复极离散低、心脏同步性较好,是选择起搏的较好部位。     

迷走神经刺激对心力衰竭兔跨室壁复极离散的影响

目的探讨迷走神经刺激对心力衰竭(简称心衰)兔跨室壁复极离散度(TDR)的影响。方法用阿霉素制作兔心衰模型,采用单相动作电位(MAP)记录技术分别记录10只开胸心衰兔(心衰组)和10只开胸正常兔(对照组)迷走神经刺激前后左室游离壁心尖上方1cm处三层心肌的MAP,测量并分析MAP时程(MAPD),TDR。结果对照组刺激前后TDR没有显著性差异,心衰组刺激后TDR显著减少(P<0.05)。迷走神经刺激前,与对照组比较,心衰组TDR明显延长(12.80±2.57ms vs8.82±1.33ms,P<0.05),刺激后两者相比无显著性差异(7.89±3.80ms vs9.44±3.21ms,P>0.05)。结论迷走神经刺激可使心衰组的TDR降低。     

跨室壁复极离散变化及其对心电图T波影响的在体实验研究

为探讨在体情况下心肌跨室壁复极离散变化及其对心电图T波影响的可能机制。运用单相动作电位 (MAP)记录技术 ,同步记录 2 1只开胸兔的左室心肌心外膜层 (Epi) ,中层 (Mid) ,内膜层 (Endo)的MAP ,分别予以减慢心率、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以及心电图T波的相应改变。结果 :①慢频率导致Mid层细胞MAP复极时间 (RT)显著延长 (从 2 0 2± 19ms到 370± 34ms,P <0 .0 5 ) ,跨壁复极离散度 (TDR)增大 (从 11± 4ms到 40± 2 1ms,P <0 .0 5 ) ,QT间期延长 (从 2 0 5± 2 1ms到 371± 30ms,P <0 .0 5 ) ,T波增宽。②dl sotalol导致Mid层细胞MAP的RT显著的延长 (从 2 0 2± 19ms到 395± 34ms,P <0 .0 5 ) ,TDR增大 (从 10± 3ms到 75± 2 5ms ,P <0 .0 5 ) ,QT间期延长 (从 2 0 8± 16ms到 397± 33ms,P <0 .0 5 ) ,三层心肌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。③ATX Ⅱ导致Mid层细胞MAP的RT显著的延长 (从370± 34ms到 473± 35ms,P <0 .0 5 ) ,TDR增大 (从 40± 2 1ms到 6 2± 19ms,P <0 .0 5 ) ,QT间期延长 (从 372± 33ms到 479± 33ms,P <0 .0 5 ) ,三层心肌MAP的 2相平台期不同程度延长 ,使复极电位梯     

急性心肌缺血犬心肌细胞瞬时外向钾电流和跨壁复极离散度变化致心律失常机制研究

目的:探讨急性心肌缺血对犬左室心肌楔形组织块瞬时外向钾电流(Ito)、跨壁复极离散度(TDR)变化及其与室性心律失常的关系。方法:建立冠状小动脉灌注犬左室心肌楔形组织块模型,应用浮置玻璃微电极和心电图同步记录技术,观察急性无灌流心肌缺血对内、中、外3层心肌细胞Ito、动作电位时程(APD)、TDR和心律失常的影响。结果:急性心肌缺血早期犬左室内、中、外3层心肌细胞的Ito增大,APD缩短,均以外膜心肌细胞最明显,TDR增加,诱发早期后除极、R-on-T期前收缩和室性心动过速。结论:急性心肌缺血时Ito增大,TDR增加,产生2相位折返,是多型性室性心动过速发生的重要机制。     

室性心动过速患者QT离散度变化的临床意义

目的　探讨室性心动过速 (VT)患者 QT离散度 (QTd)变化的意义。方法　对正常对照组 (35例 )和 VT组 (31例 )记录 12导联同步心电图 ,人工测量 QT间期 ,计算 QTd。结果　与对照组相比 ,VT组 12导联QTd明显增加 (P<0 .0 1) ,但两组之间存在很大交叉 ,无法建立正常参考值 ;QT间期明显延长 (P<0 .0 1) ,两组QTmax多见于 V2 、V3、V4 和 V5导联 (分别为 75 .0 %、77.8% ) ,两组 QTmax、QTmin导联分布无显著差异 (P>0 .0 5 )。结论　 VT患者的 QTd不能代表心肌复极的区域性差异 ,仅可作为心肌复极异常简单、粗略的指标。     

Changes of the T-wave amplitude and angle: an early marker of altered ventricular repolarization in hypertension

BACKGROUND: The heterogeneity of ventricular repolarization is an important proarrhythmic factor. QT dispersion has been proposed to reflect the inhomogeneity of ventricular repolarization, but a poor reproducibility limits its clinical applicability. Reliable noninvasive methods to quantify abnormalities in ventricular repolarization are still lacking. The T-loop morphology analysis is a novel method aimed at quantifying ventricular repolarization. HYPOTHESIS: To test the ability of the T-loop morphology analysis to discriminate between hypertensive patients and healthy subjects, 105 hypertensive patients (mean age 63.6 +/- 12.3 years) and 110 healthy controls (mean age 49.7 +/- 14.3 years) were evaluated. METHODS: The maximum QT interval (QT maximum), the minimum QT interval (QT minimum), and their difference (QT dispersion) were calculated from a digitally recorded 12-lead electrocardiogram (ECG) in both study groups. X, Y, and Z leads were reconstructed from the 12-lead ECG, and the amplitude of the maximum T vector (T amplitude) and the angle between the maximum T vector and X axis (T angle) were calculated from the projection of the T loop in the frontal plane. RESULTS: T amplitude (p < 0.001), T angle (p = 0.05), and QT dispersion (p = 0.04) were significantly different between hypertensive patients and controls, while QT maximum (p = 0.14) and QT minimum (p = 0.35) did not differ between the groups. T amplitude was the only marker which differed between hypertensive patients without ECG criteria for left ventricular hypertrophy and controls (p = 0.002). CONCLUSIONS: T-loop features and particularly T amplitude are significantly different between hypertensive patients and healthy controls and may serve as early markers of repolarization abnormalities in a hypertensive population.     

卡维地洛对扩张型心肌病跨室壁复极不均一性的影响

为观察卡维地洛对扩张型心肌病跨室壁复极不均一性的作用,将24只家兔随机分为扩张型心肌病组、卡维地洛组和正常对照组。阿霉素静脉注射8周造成扩张型心肌病模型,卡维地洛组给予口服卡维地洛8周进行干预。在体用非程序刺激方法测定三组家兔心室颤动阈值(VFT),离体测定心外膜、中层心肌和心内膜心肌细胞的单相动作电位复极90%时程(MAPD90)、跨室壁复极离散度(TDR)。结果:与正常对照组相比,扩张型心肌病组VFT明显降低(P<0.001),三层心肌细胞MAPD90均明显延长(P<0.001),中层心肌细胞较心外膜、心内膜下心肌细胞延长更为显著(P<0.05)。而卡维地洛组心外膜、心内膜MAPD90较扩张型心肌病组延长(P<0.05),但中层心肌MAPD90较扩张型心肌病组延长无明显差异(P>0.05)。与扩张型心肌病组相比,卡维地洛组TDR明显减小。结论:卡维地洛能降低扩张型心肌病的跨室壁复极不均一性,故能降低扩张型心肌病的心律失常发生率。