心室异常除极顺序与电张调整性T波的相关性研究

目的探讨心室最早异常除极点与心脏电张调整性T波产生的相关性。方法对91例（37例右心室心尖部临时或永久性起搏后，14例特发性室性心动过速终止或射频导管消融后，40例间歇或持续性预激综合征射频导管消融后）持续或间歇性心室除极异常患者的心室最早异常除极点与电张调整性T波产生的相关性进行研究，并对出现与未出现电张调整性T波的心室最早异常除极点的分布特征进行分析。结果①右心室心尖部起搏及左心室下后间隔特发性室性心动过速者lOO％出现电张调整性T波。②除少数特殊心室最早异常除极点外，预激综合征旁道下传阻断后，多数患者出现电张调整性T波。③右心室流出道室性心动过速及右希氏束旁、右前问隔、右前壁旁道下传阻断后不出现电张调整性T波。④不同部位心室最早异常除极产生的电张调整性T波的导联分布特征及其深度不同。结论不同心室异常除极顺序产生的电张调整性T波的导联分布特征及深度也不同，这些特征对与缺血性及急性肺栓塞性T波改变的鉴别有极大帮助。     

右心室心尖部起搏时QRS波群与电张调整性T波的相关性研究

目的探讨右心室心尖部起搏时QRS形态与心脏电张调整性T波的相关性。方法对35例右心室心尖部临时或永久性起搏患者起搏时QRS形态与恢复室上性心律时心脏电张调整性T波的分布特征及其相关性进行分析，并比较其同导联T／QRS比值。结果右心室心尖部起搏后电张调整性T波分布广，除下壁导联（Ⅱ、Ⅲ、aVF）外，胸导联亦广泛存在（V1-V4占100．0％，V1-V6占76，7％），倒置最深的T波常分布在V。（深度-0．71±0.27mV）；心室起搏时最大负相QRS波群常出现在Ⅲ（深度-2.16±0．39mV）；多数导联起搏时负相QRS波群深度与恢复室上性心律时同导联心脏电张调整性T波的深度呈正相关（r=-0．3454—0．4804，P〈0．05），T／QRS比值在胸导联（0．324±0，105—0．407±0．166）明显高于下壁导联（0．177±0.041—0．216±0．078，P〈0．01）。结论右心室心尖部起搏时负相QRS波群深度与同导联心脏电张调整性T波的深度呈正相关，胸导联负相QRS波群所致电张调整性T波的深度约为下壁导联的2倍。     

老年预激综合征患者射频消融术后电张调整性T波的变化规律

目的探讨老年预激综合征患者射频消融术后电张调整性T波变化规律。方法回顾性分析2011年10月至2015年11月该院确诊治疗的预激综合征老年患者200例,依据预激综合征的显隐性分为显性组和隐性组,每组100例,均给予射频消融术治疗及十二导联平静心电图检查,统计分析电张调整性T波记忆现象的发生情况及其在各个旁道发生、导联分布的特点及规律。结果显性组术后电张调整性T波检出率及记忆中倒置深度明显高于隐性组;各旁道电张调整性T波发生率明显高于隐性组,电张调整性T波多发生于距离希氏束较远的旁道(均P<0.05);显性组最大δ波时间、最大δ波百分比、T波最大深度、持续时间明显高于隐性组(P<0.05)。结论显性预激综合征患者术后更易发生T波记忆现象,且多发生于距离希氏束较远的旁道,了解该现象的导联分布特征、深度、持续时间等规律,有助于更准确鉴别不同原因所致的T波改变,避免误诊及作出相应的干预。     

电张调整性T波的研究现状

按传统概念T波异常可分为原发性改变和继发性改变。原发性T波改变是由于心室动作电位的形态或时程不均匀变化所致,激动顺序无改变,通常为病理性,偶见于心电图正常变异如Juvenile波等^[1]。继发性T波改变是因心室激动顺序改变引起T波与主波方向相反,动作电位形态或时程无改变,除极顺序正常时此种继发性T波改变瞬即消失,见于左、右束支传导阻滞,     

电张调整性T波的研究进展和临床意义

1982年Rosenhaum提出了电张调整性T波（dectrotomc modulated Twave，EMTV）变化的理论。电张调整性T波是指心脏为了适应异常的心室内激动顺序，通过电张调整机制使T波与QRS波群主波同相，具有电张调整作用、心脏记忆现象和累积作用。电张调整性T波变化的机理，目前尚不十分清楚。     

电张调整性T波改变的临床观察

26例显性预激综合征消融后 ,5例特发性室性心动过速终止后及 2 2例VVI起搏恢复自主心律后显示不同程度电张调整性T波改变 ,前二者持续约 1周 ,后者持续约 2周 ,均未经治疗自动恢复正常。结论 :电张调整性T波改变是心肌正常的电生理特性 ,一般持续 1～ 2周后自动恢复正常。     

不同原因电张调整性T波的导联分布特征

目的探讨不同原因电张调整性T波改变的心电学特征。方法对30例右心室心尖部临时或永久性起搏后、10例左室下后间隔特发性室性心动过速后及8例后间隔间歇性或持续性预激综合征射频消融术后电张调整性T波的分布特征进行分析。结果①电张调整性T波的导联分布特点为:右心室心尖部起搏组分布最广,除下壁导联(Ⅱ、Ⅲ、aVF)外,胸导联(Vl￣V4100.0%,Vl￣V676.7%)亦广泛存在,其最大倒置T波的深度(0.85±0.26mV)较特发性室性心动过速组(0.42±0.18mV)、预激综合征组(0.40±0.19mV)均深,差异有非常显著性意义(P均<0.01),最深倒置的常分布在V3、V4导联。②特发性室性心动过速组分布也较广,除下壁导联外,左胸导联(V4￣V6为100.0%)亦存在,其最深倒置的常分布在V4、V5导联。③预激综合征组分布较窄,常局限于下壁导联。结论不同原因电张调整性T波的导联分布也不同,了解这些特征有助于与心肌缺血、急性肺栓塞等所致的T波改变相鉴别。     

电紧张调整性T波改变的临床观察

目的 :观察各种原因所致电张调整性T波改变的临床表现和持续时间。方法 :对显性预激射频消融后 5 8例、特发性室性心动速终止后 5例及右室起搏 （VVI）恢复自主心律后 2 6例的进行动态心电图观察。结果 :显性预激消融后 2 6例 ,特发性室性心动速终止后 5例及VVI起搏恢复自主心律后 2 2例显示不同程度电张调整性T波改变 ,前二者持续约 1周 ,后者持续约 2周 ,均未经治疗自动恢复正常。结论 :电张调整性T波改变是心肌正常的电生理特性 ,一般持续 1～ 2周自动恢复正常。     

右侧显性旁道射频消融术后电张调整性T波一例

患者男性,23岁,因体格检查发现预激综合征1年入院。入院心电图提示B型预激综合征,行射频消融术后复查心电图δ波消失,Ⅱ、Ⅲ、aVF导联T波倒置,20天后复查心电图恢复正常。患者射频消融术后心电图改变考虑电张调整性T波。     

预激综合征射频消融术后心电图电张调整性T波及J-ST段特征分析

目的探讨预激综合征射频消融房室旁道后心电图出现电张调整性T波及J-ST段的特征及其发生机制。方法45例持续性预激综合征患者，对比射频消融术前后心电图，总结和分析术后电张调整性T波、J波以及ST段变化的发生规律和特征。结果45例中射频消融术后出现电张调整性T波改变有27例，间隔部和左前壁旁道消融后电张调整性T波出现率最高（达100％），电张调整性T波主要分布于下壁导联（Ⅱ、Ⅲ、aVF）和高侧壁导联（Ⅰ、aVL）；下壁导联电张凋整性T波倒置深度Ⅲ〉aVF〉Ⅱ（P〈0．01），高侧壁导联aVL〉Ⅰ。此外尚可出现J-ST改变，表现为J点抬高、J波和ST段水平或弓背向下型抬高，总发生率高于同期隐匿性旁道消融组（42．2％vs3．5％，P〈0．01）。结论预激综合征射频消融术后电张调整性T波的出现取决于预激时QRS波形态；射频消融术后心电图可出现类似早期复极综合征的J-ST段改变。     

Transient T Wave Abnormalities After Cessation of Ventricular Preexcitation: Memory of What?

T Wave Memory? (1) Ventricular preexcitation causes both secondary and primary T wave changes. The secondary changes disappear immediately after cessation of preexcitation (ablation of accessory pathways) and unmask the primary T wave changes that regress within days, weeks, or months. (2) The pattern of primary T wave change produced by ventricular preexcitation depends on the location of the accessory pathway connections. The septal and posterior connections are associated with more prominent anteriorly directed T wave deflections and deviation of the T wave vector superiorly. The left lateral connections are associated with rightward deviation of the T wave vector in the frontal plane. (3) The primary T wave abnormalities are believed to be caused by local lengthening of repolarization, but the site of the postulated abnormalities needs to be established. (4) The persistence and slow dissipation of the primary T wave change induced by ventricular pacing, left bundle branch block, and presumably ventricular preexcitation have been attributed to the memory of past events. The nature of these events is not known. Several in vitro models demonstrated phenomena of gradual adjustment of ventricular action potential duration to change in cycle length, or to altered pattern of stimulation, but none of such models has mimicked the long-lasting regression of T wave abnormalities. (5) The terms T wave memory and pseudoprimary repolarization changes lack specificity and are unnecessary additions to the electrocardiographic vocabulary.     

Electrotonic Inhibition and Active Facilitation of Excitability in Ventricular Muscle

Inhibition and Facilitation in Cardiac Muscle. Introduction: The effects of subthreshold electrical pulses on the response to subsequent stimulation have been described previously in experimental animal studies as well as in the human heart. In addition, previous studies in cardiac Purkinje fibers have shown that diastolic excitability may decrease after activity (active inhibition) and, to a lesser extent, following subthreshold responses (electrotonic inhibition). However, such dynamic changes in excitability have not been explored in isolated ventricular muscle, and it is uncertain whether similar phenomena may play any role in the activation pal-terns associated with propagation abnormalities in the myocardium. Methods and Results: Experiments were performed in isolated sheep Purkinje fibers and papillary muscles, and in enzymatically dissociated guinea pig ventricular myocytes. In all types of preparations introduction of a conditioning subthreshold pulse between two subthreshold pulses was followed by a transient decay in excitability (electrotonic inhibition). The degree of inhibition was directly related to the amplitude and duration of the conditioning pulse and inversely related to the postconditioning interval. Yet, inhibition could be demonstrated long after (> 1 sec) the end of the conditioning pulse. Electrotonic inhibition was found at all diastolic intervals and did not depend on the presence of a previous action potential. In Purkinje fibers, conditioning action potentials led to active inhibition of subsequent responses. In contrast, in muscle cells, such action potentials had a facilitating effect (active facilitation). Electrotonic inhibition and active facilitation were observed in both sheep ventricular muscle and guinea pig ventricular myocytes. Accordingly, during repetitive stimulation with pulses of barely threshold intensity, we observed: (1) bistability (i.e., with the same stimulating parameters, stimulus: response patterns were either 1:1 or 1:0, depending on previous history), and (2) abrupt transitions between 1:1 and 1:0 (absence of intermediate wenckebach-like patterns). Simulations utilizing an ionic model of cardiac myocytes support the hypothesis that electrotonic inhibition in well-polarized ventricular muscle is the result of partial activation of I_k following subthreshold pulses. On the other hand, active facilitation may be the result of an activity-induced decrease in the conductance of I_K1. Conclusion: Diastolic excitability of well-polarized ventricular myocardium may be transiently depressed following local responses and transiently enhanced following action potentials. On the other hand, diastolic excitability decreases during quiescence. Active facilitation and electrotonic inhibition may have an important role in determining the dynamics of excitation of the myocardium in the presence of propagation abnormalities.     

不同起搏部位对左心室功能影响的对比研究

目的对比不同起搏部位对左心室功能影响。方法将植入永久心脏起搏器手术患者130例根据起搏部位不同分为A组(右室心尖部,35例)、B组(右室高位间隔面,25例)、C组(右室中位间隔面,28例)、D组(右室低位间隔面,32例)。比较四组患者术前和术后1.5年左心室射血分数(LVEF)、左心室舒张末期容积(LVEDV)、血清N端B型脑钠肽前体(NT-pro BNP)、QRS波群时限、心血管事件发生情况。结果与术前比较,A组术后1.5年LVEF降低(P0.05),A、D组患者术后LVEDV有不同程度增加;术后1.5年四组患者LVEDV比较,A组最大(P0.05)。与术前比较,A、B、D组术后NT-pro BNP均有不同程度增加;术后1.5年四组患者NT-pro BNP比较,A组最大(P0.05)。术后1.5年四组患者QRS波群时限比较,A组最宽,C组最窄(P0.05)。C组患者心血管事件发生率(3.6%)低于A组(40.0%)及D组(21.9%)(P0.05)。结论右室中位间隔面起搏对左心室功能影响小,心血管事件发生率低,可作为植入永久心脏起搏器的最佳部位。     

Phenylephrine Increases T Wave Shock Energy Required to Induce Ventricular Fibrillation

Phenylephrine Increases VFT. Introduction : Previous reports in experimental models have suggested that ventricular fibrillation threshold (VFT) can be changed by manipulating cardiac neural tone using agents such as phenylephrine. The purpose of this study was to determine whether phenylephrine increased the energy required to induce VF in humans undergoing such induction using DC energy applied to the T wave.
Methods and Results : In this prospective investigation, 18 consecutive patients with previously implanted cardioverter defibrillators had induction of VF by placing DC monophasic shocks into the T wave coupled 310 msec after the eighth paced ventricular complex at 400 msec. The T wave shock energy was titrated from 0.2 to 12 J until sustained VF or ventricular tachycardia was induced. Phenylephrine was infused either before the first or second VF induction in a randomized fashion to increase systolic blood pressure by more than 20 mmHg. The mean energy required to induce VF was 1.1 J at baseline and increased to 1.7 J during phenylephrine infusion (P = 0.036). The mean arterial pressure increased from 88 to 114 mmHg (P < 0.001), and the mean sinus cycle length increased from 850 to 1070 msec (P < 0.001). Ten of 13 (77%) patients with sinus cycle length prolongation bad increased energy requirements to induce VF compared with only 1 of 5 patients (20%) without sinus cycle length prolongation (P < 0.05).
Conclusion : Phenylephrine increases VFT in humans presumably by reflex activation of the baroreceptors decreasing sympathetic and/or increasing parasympathetic cardiac efferent effects.     

Electrotonic modulation of the T wave and cardiac memory

Alterations in the sequence of ventricular activation (left bundle branch block occurring spontaneously or induced by atrial pacing; right ventricular pacing) were studied and shown to induce two opposite changes in the order of ventricular repolarization. One, which causes classic secondary T wave changes, occurs and disappears instantaneously, and is proportional in magnitude to the QRS complex but of opposite direction. The other, which requires a long time to reach its maximal effect and to be dissipated, shows the same direction as the abnormal QRS forces but becomes apparent only when normal activation is restored. The former is a well known consequence of prolongation of the activation time, but the latter appears to be modulated by electrotonic interactions occurring during cardiac activation, in such a way that repolarization is delayed in sites where depolarization begins, and accelerated in sites where depolarization terminates. Our study suggests that electrotonically modulated T wave changes show accumulation and memory, and may persist for days or weeks after the provoking stimulus (the change in the activation sequence) is discontinued. The fact that any shift of the activation sequence may produce “pseudoprimary” T wave changes that may persist long after cessation of the triggering factor has wide clinical implications. Electrotonic modulation of ventricular repolarization is a basic electrophysiologic mechanism that may account for several features of normal and abnormal T waves, and for the possible existence of a heart memory.     

特发性室性心动过速后的电张调整性T波变化

部分特发性室性心动过速(以下简称特发性室速)在心动过速终止后可出现明显的T波改变,易误诊为心肌缺血。现将我们有连续心电图观察的2例病人报道如下: 例1 患者,女,14岁。因阵发心悸、上腹痛6个月,持续发作1天入院。6月前因上述症状入院,心室率206次/分,误诊为阵发性室上性心动过速,予以电转后复律,心电图示Ⅱ、Ⅲ、avF、V_4～V_5T波倒置,但未作连续观察,心脏B     

Postmyocardial Infarction Patients Susceptible to Ventricular Tachycardia Show Increased T Wave Dispersion Independent of Delayed Ventricular Conduction

Arrhythmia Markers After Myocardial Infarction. Introduction: Experimentally, both delayed ventricular conduction and nonhomogeneous ventricular repolarization contribute to reentrant arrhythmias. We tested the hypothesis that increased T wave dispersion is independent of delayed ventricular conduction associated with arrhythmia vulnerability in postmyocardial infarction (post-MI) patients.
Methods and Results: We studied 32 post-MI patients with clinical or inducible monomorphic ventricular tachycardia (VT group), 28 post-MI patients without arrhythmias (MI group), and 13 healthy controls, using magnetocardiographic (MCG) mapping with signal averaging. Twelve-lead ECG was the reference. Filtered QRS duration (fQRS) and T wave peak to T wave end interval (TPE) were used as measures of ventricular conduction and nonhomogeneity in ventricular repolarization, respectively. In MCG, the VT group showed the longest fQRS (  135 ± 34  msec vs  114 ± 22  msec in the MI group;  P = 0.012  ). Mean TPE and maximum TPE in VT versus MI groups were  78 ± 9  msec versus  70 ± 6  msec (  P < 0.001  ) and  117 ± 23  msec versus  104 ± 19  msec (  P = 0.020  ), respectively. Maximum TPE did not correlate with fQRS in the VT group (  r = 0.063; P = NS  ) but did correlate in the MI group (  r = 0.396; P = 0.037  ). For identification of post-MI patients prone to VT, selection of cutoff values for fQRS > 140 msec and mean TPE > 81 msec gave sensitivity and specificity of 41% and 89%, and 31% and 96%, respectively. Their combination increased sensitivity to 63% while maintaining 89% specificity.
Conclusion: Post-MI patients susceptible to VT show increased T wave dispersion independent of delayed ventricular conduction.     

急性心肌梗死后T波极性变化与左心功能的关系

目的探讨Q波性心肌梗死从急性期到慢性期心肌损害、心功能与T波方向变化的关系.方法选择急性前壁心肌梗死病人93例,持续T波倒置组44例,T波直立组49例,按T波恢复直立的时间不同又分4个亚组:＜3月组6例;(3～6)月组16例;(6～12)月组23例;持续直立组4例.测量各组的左室射血分数、舒张末径、室壁运动记分等超声心动图指标.结果除持续T波直立亚组外,其他T波直立亚组的左室射血分数高于T波倒置组,左室舒张末径、室壁运动记分低于T波倒置组.结论早期T波由倒置变为直立的病人,左心功能改善显著;有Q波的导联倒置T波正常化的早晚可以用来评估左心功能.     

Mechanism of Ventricular Tachycardia Termination by Pacing at Left Ventricular Sites in Patients with Coronary Artery Disease

Objective: The mechanism by which pacing terminates ventricular tachycardia (VT) may depend on the location of the pacing site relative to the reentry circuit. The purpose of this study was to compare the mechanisms by which pacing terminates VT at left ventricular (LV) sites with and without concealed entrainment (CE) in patients with prior myocardial infarction. Methods and Results: LV mapping was performed in 29 patients (26 men, 3 women, mean age 67±11 years, ejection fraction 0.28±0.11) with 55 hemodynamically-tolerated VTs (mean cycle length 478±92 msec). A total of 408 pacing trains were delivered at 102 sites with CE. Radiofrequency catheter ablation was successful in 41 of 55 VT's. At sites with concealed entrainment, VT was terminated by pacing at 17/41 (41%) successful and at 4/61 (7%) unsuccessful ablation sites (p<0.01). Termination without global ventricular capture was the most frequent termination mode (10/21), followed by termination with orthodromic (4/21) and non-orthodromic capture (7/21). Conclusion: In patients with prior myocardial infarction, pacing at sites of CE during VT usually terminates VT either without global capture or by orthodromic capture. Termination of VT by pacing without global capture or with orthodromic capture at sites of CE suggests that the site is within a critical area of the reentry circuit.