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.     

Long-term cardiac memory in canine heart is associated with the evolution of a transmural repolarization gradient

OBJECTIVE: The contribution of regional electrophysiologic heterogeneity to the T-wave changes of long-term cardiac memory (CM) is not known. We mapped activation and repolarization in dogs after induction of CM and in sham animals. METHODS AND RESULTS: CM was induced by three weeks of AV-sequential pacing at the anterior free wall of the left ventricle (LV), midway between apex and base in 5 dogs. In 4 sham controls a pacemaker was implanted but ventricular pacing was not performed. At 3 weeks, unipolar electrograms were recorded (98 epicardial, 120 intramural and endocardial electrodes) during atrial stimulation (cycle length 450 ms). Activation times (AT) and repolarization times (RT) were measured and activation recovery intervals (ARIs) calculated. CM was associated with 1) deeper T waves on ECG, with no change in QT interval; 2) longer activation time at the site of stimulation in CM (29.7+/-1.0, X+/-SEM) than sham (23.9+/-1.3 ms p<0.01); 3) an LV transmural gradient in repolarization time such that repolarization at the epicardium terminated 12.4+/-2.4 ms later than at the endocardium p<0.01), in contrast to no gradient in shams (2.7+/-4.2 ms); in memory dogs, the repolarization time gradient was greatest at sites around the pacing electrode varying from 13.1+/-2.3 ms to 25.5+/-3.8 ms; 4) more negative left ventricular potentials at the peak of the body surface T wave (-4.9+/-0.8 vs -2.2+/-0.4 mV; p<0.05) but no altered right ventricular epicardial T-wave potentials. ARIs did not differ between groups. Right ventricular activation was delayed but was not associated with altered repolarization because of compensatory shortening of the right ventricular ARIs. CONCLUSION: CM-induced T-wave changes are caused by evolution of transmural repolarization gradients manifested during atrial stimulation that are maximal near the site of ventricular pacing.     

不同部位左心室内膜与外膜起搏对心力衰竭心脏的电生理作用差异

目的 评估左心室不同部位心内膜与外膜起搏对心力衰竭（心衰）犬心脏的电激动同步性以及复极离散度的影响及其差异.方法 12只比格犬,体重（12.5±1.7）kg.使用随机数字法平均分为2组（正常组和心衰组）.利用右心室心尖部快速起搏制作慢性心衰模型.左心室放置64极篮状电极导线进行电生理标测.通过左心室不同部位起搏（心底部心内膜与心外膜,心尖部心内膜与心外膜）记录并测量体表12导联心电图的QT间期、T波峰点与T波下降支最大斜率处切线与等电位线交点（Tp-e）间期,同时测定左心室心内膜整体激动时间以及各篮状电极记录的激动恢复间期及其复极离散度.结果 基础状态下,与正常心脏相比,心衰组QT间期、T波顶点与T波终点之间的时限Tp-e间期以及激动恢复间期均延长（P＜0.05）.心衰组中,与左心室心内膜起搏相比,相同部位的心外膜起搏时的QT和Tp-e间期均显著延长[QT：心底部（270±13）ms对（255±15）ms,（P＜0.01）;心尖部（275±12）ms对（257±11）ms,（P＜0.01）;Tp-e：心底部（50.2±8.3） ms对（42.7±4.5） ms,（P＜0.01）;心尖部,（52.9±10.1）ms对（45.6±9.3）ms,（P＜0.01）].心室激动恢复间期离散度无论在左心室心内膜还是在心外膜,近心底部起搏时较近心尖部起搏时显著减小.[心内膜起搏（4.1±0.5） ms对（5.8±0.7）ms,（P＜0.05）;心外膜起搏（4.7±0.6） ms对（6.2±0.9） ms,（P＜0.05）].在心衰心脏,左心室心外膜起搏时,左心室整体心内膜平均激动时间较心内膜起搏时明显延长（42.9±5.9）ms对（26.1±4.0）ms,（P＜0.001）].结论 左心室心内膜起搏较心外膜起搏有更好的心脏激动电同步性.心衰后,左心室心外膜起搏较心内膜起搏可致更长的复极时间以及更大的复极离散度.本研究结果提示左心室心内膜起搏较心外膜起搏可产生更好的电生理效应,有可能降低心衰心脏再     

Dispersion of repolarization in cardiac resynchronization therapy

BACKGROUND: Proarrhythmic effects of cardiac resynchronization therapy (CRT) as a result of increased transmural dispersion of repolarization (TDR) induced by left ventricular (LV) epicardial pacing in a subset of vulnerable patients have been reported. The possibility of identifying these patients by ECG repolarization indices has been suggested. OBJECTIVES: The purpose of this study was to test whether repolarization indices on the ECG can be used to measure dispersion of repolarization during pacing. METHODS: CRT devices of 28 heart failure patients were switched among biventricular, LV, and right ventricular (RV) pacing. ECG indices proposed to measure dispersion of repolarization were calculated. The effects of CRT on repolarization were simulated in ECGSIM, a mathematical model of electrocardiogram genesis. TDR was calculated as the difference in repolarization time between the epicardial and endocardial nodes of the heart model. RESULTS: Patients: The interval from the apex to the end of the T wave was shorter during biventricular pacing (102 +/- 18 ms) and LV pacing (106 +/- 21 ms) than during RV pacing (117 +/- 22 ms, P < or =.005). T-wave amplitude and area were low during biventricular pacing (287 +/- 125 microV and 56 +/- 22 microV.s, respectively, P = .0006 vs RV pacing). T-wave complexity was high during biventricular pacing (0.42 +/- 0.26, P = .004 vs RV pacing). Simulations: Repolarization patterns were highly similar to the preceding depolarization patterns. The repolarization patterns of different pacing modes explained the observed magnitudes of the ECG repolarization indices. Average and local TDR were not different between pacing modes. CONCLUSION: In patients treated with CRT, ECG repolarization indices are related to pacing-induced activation sequences rather than transmural dispersion. TDR during biventricular and LV pacing is not larger than TDR during conventional RV endocardial pacing.     

Effects of sudden changes in cycle length and pacing site on canine cardiac surface QRST isoarea maps

The effects of changes in paced cycle length alone and changes in both paced cycle length and site of pacing on canine cardiac surface QRST isoarea maps were studied. The correlations between QRST isoarea maps acquired during right ventricular pacing at 900 ms and 700 ms averaged 0.97. The correlations between maps acquired during RV pacing at 900 ms and 500 ms averaged 0.94. The root mean square value of QRST areas progressively decreased as cycle length was decreased from 900 ms to 700 ms and then to 500 ms. This suggests that the pattern of distribution of repolarization properties remained the same and the magnitude of difference in repolarization properties decreased as cycle length was decreased. The correlation coefficients of QRST isoarea maps acquired during RV pacing at 900 ms and those acquired during left ventricular pacing at 700 ms and 500 ms averaged 0.74 +/- 0.01 and 0.68 +/- 0.03, respectively. These correlations were lower than those associated with a change in pacing cycle length alone. Root mean square differences in QRST areas recorded during changes in both pacing site and pacing cycle length were greater than the differences associated with change in cycle length alone. This suggests that changes in activation sequence altered repolarization properties more than they were altered by changes in cycle length alone. QRST isoarea maps have been proposed for assessing arrhythmia vulnerability. The results of this study provide a framework for interpreting QRST isoarea maps acquired during supraventricular tachycardias, premature ventricular complexes, and sustained ventricular tachycardias.     

心脏再同步治疗对心肌复极离散度的影响

目的观察心室不同位点起搏时心电图上心肌复极标志的变化,了解以双心室起搏技术为核心的心脏再同步治疗（CRT）对心肌复极离散的影响。方法 入选接受CRT植入的患者在起搏器植入后1周内记录12导联心电图,分别将起搏器程控为无起搏、右心室内膜下起搏（RV—EndoP）、左心室外膜起搏（LV—EpiP）及双心室同步起搏（BivP）四种不同状态并记录心电图。阅读不同起搏位点时的QRS时限、QT问期及TP-E时限。QTc用Bazett公式[QTc=实测QT／（RR）1／2]进行矫正。结果基线QYc为（489．2±51．2）ms,而RV—EndoP、LV—EpiP起搏导致QR明显延长[RV-EndoP（537．3±45．7）ms,P〈0．05;LV—EpiP（592．4±60．2）ms,P〈0．001],而BivP起搏为（491．3±52．7）ms,P〉0．05;基线TP．F（113．8±15．7）ms,RV-EndoP、LV—EpiP均导致TP-E明显延长[RV．EndoP（124．8±24．7）ms,P〈0．05;LV．EpiP（133．3±37．8）ms,P〈0．005],BivP时TP-E时限为（109．9±17．1）ms,有轻度缩短,但差异没有统计学意义（P〉0．05）。结论左心室外膜起搏可明显延长心肌复极离散指标;双心室同步起搏可减少由单纯左心室外膜起搏引起的复极离散度的增大。     

Dispersion of the monophasic action potential duration in patients with polymorphic ventricular tachycardia.

The mechanism of polymorphic ventricular tachycardia (PMVT) remains unclear. To investigate the electrophysiologic mechanism of PMVT, monophasic action potentials (MAPs) were recorded with a contact electrode technique from right ventricular sites during sinus rhythm and right ventricular pacing. MAPs were obtained from 6 patients with PMVT (PMVT group) and 11 patients without PMVT (control group). The duration from the onset of the upstroke to 90% repolarization of the MAP (MAPD90) during right ventricular pacing at both pacing cycle lengths of 600 and 400 ms was significantly longer in the PMVT group than in the control group (332+/-60 ms vs 279+/-33 ms [P < .005] and 276+/-32 ms vs 229+/-23 ms [P < .0001], respectively). Dispersion of the MAPD90 in sinus rhythm was significantly larger in the PMVT group than in the control group (52.5+/-34.6 ms vs 26.1+/-12.0 ms [P < .005]), and dispersion of the MAPD90 during right ventricular pacing at both pacing cycle lengths of 600 and 400 ms was also significantly larger in the PMVT group than in the control group (86.0+/-44.2 ms vs 37.4+/-28.6 ms [P < .005], and 48.8+/-19.3 ms vs 27.1+/-7.1 ms [P < .05], respectively). Dispersion of repolarization time (activation time plus MAPD90) at a pacing cycle length of 600 ms was longer in the PMVT group than in the control group (104.3+/-38.9 ms vs 49.4+/-31.2 ms [P < .05]). These results suggest that the patients with PMVT have a greater regional dispersion of ventricular repolarization time and that the heterogeneity of ventricular repolarization may play an important role in the genesis of PMVT.     

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.     

Impact of left ventricular epicardial and biventricular pacing on ventricular repolarization in normal-heart individuals and patients with congestive heart failure.

AIMS: Malignant ventricular arrhythmias can arise in a subset of congestive heart failure (CHF) patients after they undergo cardiac resynchronization therapy (CRT), thus counteracting the haemodynamic benefits typically associated with biventricular pacing. This study seeks to assess whether alteration of the ventricular transmural repolarization and conduction due to reversal of the depolarization sequence during epicardial or biventricular pacing facilitate the development of ventricular arrhythmias. METHODS AND RESULTS: ECGs and monophasic action potential (MAP) were recorded during programmed stimulation from right ventricle (RV) endocardium (RV-Endo), left ventricle (LV) epicardium (LV-Epi), or both (biventricular, Bi-V) in 15 individuals without structural heart diseases. In patients with severe CHF and CRT (n=21), ECGs were collected during RV-Endo, LV-Epi, and Bi-V pacing. MAP duration on intracardiac electrogram, the QT, JT, and T(peak)-T(end) intervals on ECGs at different pacing sites were measured and compared. In subjects with or without structural heart disease, compared with RV-Endo pacing, LV-Epi and Bi-V pacing resulted in a longer JT (341.78+/-61.97 ms with LV-Epi, 325.86+/-59.69 ms with Bi-V vs. 286.14+/-38.68 ms with RV-Endo in CHF individuals, P<0.0001) or T(peak)-T(end) interval (121.55+/-19.88 ms with LV-Epi, 117.71+/-42.63 ms with Bi-V vs. 102.28+/-12.62 ms with RV-Endo in normal-heart subjects, P<0.0001; 199.70+/-62.44 ms with LV-Epi, 184.89+/-74.08 ms with Bi-V vs. 146.41+/-31.06 ms with RV-Endo in CHF patients, P<0.0001), in addition to prolonged myocardial repolarization time and delayed endocardial activation. During follow-up, sudden death and arrhythmia storm occurred in two CHF patients after CRT. CONCLUSION: Epicardial and biventricular pacing prolong the time and increase the dispersion of myocardial repolarization and delay the transmural conduction. All of these should be considered as potential arrhythmogenic factors in CHF patients who receive CRT.     

Effects of the class III antiarrhythmic drug dofetilide on ventricular monophasic action potential duration and QT interval dispersion in stable angina pectoris.

The effects of intravenous dofetilide on ventricular monophasic action potential duration and effective refractory period at the right ventricular apex and outflow tract were studied in 18 patients (aged 37 to 70 years) with ischemic heart disease. Six patients received low-dose dofetilide as a 3 micrograms/kg loading dose over 15 minutes and a 1.5 micrograms/kg maintenance dose over 45 minutes; 6 received high-dose dofetilide 6 + 3 micrograms/kg and 6 placebo. During atrial pacing at a cycle length of 800 ms high-dose dofetilide prolonged right ventricular apex monophasic action potential duration by 45 ms (16%) and the effective refractory period by 40 ms (16%). At the right ventricular outflow tract, monophasic action potential duration was prolonged by 45 ms (15%) and effective refractory period by 55 ms (21%). During atrial pacing at a cycle length of 500 ms high-dose dofetilide prolonged the right ventricular apex monophasic action potential duration by 40 ms (18%) and the effective refractory period by 43 ms (21%). The right ventricular outflow tract monophasic action potential duration was prolonged by 33 ms (14%) and effective refractory period by 45 ms (21%). Dofetilide produced no increase in the dispersion of repolarization between the 2 sites. During the maintenance infusion QTc prolongation by high-dose dofetilide averaged 43 ms (10%) with no increase of interlead QT dispersion. The effects of dofetilide on QT interval and effective refractory period are shown to be due to a direct effect on action potential duration with no effect on dispersion. No rate dependence of monophasic action potential prolongation was detected at these cycle lengths.     

Dispersion of repolarization in canine ventricle and the electrocardiographic T wave: Tp-e interval does not reflect transmural dispersion

BACKGROUND: The concept that the interval between the peak (T(peak)) and the end (T(end)) of the T wave (T(p-e)) is a measure of transmural dispersion of repolarization time is widely accepted but has not been tested rigorously by transmural mapping of the intact heart. OBJECTIVES: The purpose of this study was to test the relationship of T(p-e) to transmural dispersion of repolarization by correlating local repolarization times at endocardial, midmural, and epicardial sites in the left and right ventricles with the T wave of the ECG. METHODS: Local activation times, activation-recovery intervals, and repolarization times were measured at 98 epicardial sites and up to 120 midmural and endocardial sites in eight open-chest dogs. In four of the dogs, long-term cardiac memory was induced by 3 weeks of ventricular pacing at 130 bpm because previous data suggest that, in this setting, delayed epicardial repolarization increases transmural dispersion. The other four dogs were sham operated. RESULTS: In sham dogs, T(p-e) was 41 +/- 2.2 ms (X +/- SEM), whereas the transmural dispersion of repolarization time was 2.7 +/- 4.2 ms (not significant between endocardium and epicardium). Cardiac memory was associated with evolution of a transmural gradient of 14.5 +/- 1.9 ms (P <.02), with epicardium repolarizing later than endocardium. The corresponding T(p-e) was 43 +/- 2.3 ms (not different from sham). In combined sham and memory dogs, T(p-e) intervals did not correlate with transmural dispersion of repolarization times. In contrast, dispersion of repolarization of the whole heart (measured as the difference between the earliest and the latest moment of repolarization from all left and right ventricular, endocardial, intramural, and epicardial recording sites) did correlate with T(p-e) (P <.0005, r = 0.98), although the latter underestimated total repolarization time by approximately 35%. The explanation for this finding is that parts of the heart fully repolarize before the moment of T(peak). CONCLUSION: T(p-e) does not correlate with transmural dispersion of repolarization but is an index of total dispersion of repolarization.     

Activation and repolarization of the normal human heart under complete physiological conditions

Knowledge of normal human cardiac excitation stems from isolated heart or intraoperative mapping studies under nonphysiological conditions. Here, we use a noninvasive imaging modality (electrocardiographic imaging) to study normal activation and repolarization in intact unanesthetized healthy adults under complete physiological conditions. Epicardial potentials, electrograms, and isochrones were noninvasively reconstructed. The normal electrophysiological sequence during activation and repolarization was imaged in seven healthy subjects (four males and three females). Electrocardiographic imaging depicted salient features of normal ventricular activation, including timing and location of the earliest right ventricular (RV) epicardial breakthrough in the anterior paraseptal region, subsequent RV and left ventricular (LV) breakthroughs, apex-to-base activation of posterior LV, and late activation of LV base or RV outflow tract. The repolarization sequence was unaffected by the activation sequence, supporting the hypothesis that in normal hearts, local action potential duration (APD) determines local repolarization time. Mean activation recovery interval (ARI), reflecting local APD, was in the typical human APD range (235 ms). Mean LV apex-to-base ARI dispersion was 42 ms. Average LV ARI exceeded RV ARI by 32 ms. Atrial images showed activation spreading from the sinus node to the rest of the atria, ending at the left atrial appendage. This study provides previously undescribed characterization of human cardiac activation and repolarization under normal physiological conditions. A common sequence of activation was identified, with interindividual differences in specific patterns. The repolarization sequence was determined by local repolarization properties rather than by the activation sequence, and significant dispersion of repolarization was observed between RV and LV and from apex to base.     

不同起搏部位对正常人体心肌复极离散的影响

目的 :观察正常人心脏不同部位或 2个部位同时起搏时的电生理及心室肌复极差异的变化。方法 :15例接受射频消融术后的患者 ,常规检查排除器质性心脏病。经冠状静脉窦将 1根标测电极送至左心室表面静脉分支 ,另 1根Pacing MAP电极送达右室心尖部 ,记录局部单向动作电位 (MAP)。分别起搏左心室心外膜、右心室心内膜及上述两部位同时起搏 ,行S1S1、S1S2 程序刺激。记录测量QRS波时限、QT间期、Tp Te 间期、MAP时程 (MAPD)等指标及心律失常事件。结果 :体表心电图上QT间期、Tp Te 间期在左室心外膜起搏 (376 .2 6ms、12 2 .5 9ms)、双心室起搏 (36 6 .4 2ms、12 4 .2 3ms)明显较右心室心内膜起搏 (349.33ms、10 4 .14ms)延长 (P <0 .0 1) ,伴有右室心尖部局部MAPD的相应变化。在相同总阵次的程序刺激中 ,左室心外膜起搏与双心室起搏时的室性心律失常多于右室心内膜起搏时 (P <0 .0 5 )。结论 :左室心外膜参与起搏后可能会增大心室肌的跨室壁复极差异 ,伴有复极时间的延长 ,从而使室性心律失常易于发生。     

左心室心外膜不同部位起搏对心室不应期离散度的影响

目的:通过模拟心脏再同步治疗中左室电极在左心室心外膜不同部位起搏情况,观察不同部位起搏对心室不应期离散度的影响。方法:采用6只犬开胸,在其左心室前侧壁心外膜缝上1块含有144(12×12)个单极电极(电极间距2 mm)的电极板。选取位于电极板对角处的2个起搏部位(左上角靠近心底部,右下角靠近心尖部),采用连续起搏方法,记录起搏周期为300 ms时整个电极板上每个单极电极上的激动恢复间期,通过其标准差及变异系数评估不应期离散度。结果:近心底部与近心尖部起搏时起搏阈值及心室激动恢复间期无显著差异[起搏阈值(0.34±0.22)mA比(0.26±0.05)mA;激动恢复间期(144.3±12.4)ms比(147.7±14.8)ms,均P>0.05]。但是,近心底部位起博的不应期离散度较近心尖部起搏的不应期离散度显著减小[标准差(4.3±0.8)ms比(5.8±0.7)ms,P<0.01;变异系数(0.030±0.006)比(0.039±0.005),P<0.01]。结论:在心脏再同步治疗左室电极植入过程中,选择恰当的左室电极植入部位有利于降低不应期离散度。     

Dispersion of monophasic action potential duration: demonstrable in humans after premature ventricular extrastimulation but not in steady state.

Abnormal dispersion of repolarization may contribute to the arrhythmogenic physiologic substrate of ventricular arrhythmia. Geographic dispersion of monophasic action potential duration was determined in steady state (drive cycle lengths 600 and 430 ms) between widely spaced right ventricular endocardial sites (geographic dispersion) in 10 control patients with right ventricular disease and complicating ventricular tachycardia (n = 9), 6 patients with right and left ventricular disease and complicating ventricular tachycardia and 7 patients with ischemic heart disease and complicating ventricular tachycardia. No significant difference in geographic dispersion could be demonstrated among the groups. Difference of monophasic action potential duration at adjacent right ventricular endocardial sites (adjacent dispersion) was determined after ventricular extrastimulation during construction of simultaneous electrical restitution curves in the same patient groups. Maximal adjacent dispersion over the electrical restitution curve was compared between disease and control groups. There was a significant difference in observations of maximal adjacent dispersion in patients with right ventricular disease and complicating ventricular tachycardia (range 5 to 85 ms, median 22.5; 14 pairs of sites; p less than 0.05) and patients with right and left ventricular disease and complicating ventricular tachycardia (range 5 to 50 ms, median 17.5; 14 pairs of sites; p less than 0.05) compared with control patients (range 5 to 20 ms, median 10; 15 pairs of sites). This difference was not evident when patients with ischemic heart disease and complicating ventricular tachycardia (range 5 to 25 ms, median 12.5; 12 pairs of sites) were compared with control patients. Maximal percent monophasic action potential shortening from steady state was significantly greater (p less than 0.001) in both groups with greater adjacent dispersions, and prolongation of activation time at monophasic action potential recording sites after premature extrastimulation tended to be greater in patients with right or right and left ventricular disease and complicating ventricular tachycardia. It is concluded that in disease, exaggeration of monophasic action potential shortening after premature ventricular extrastimulation may contribute to the electrophysiologic arrhythmogenic substrate.     

G-CSF therapy reduces myocardial repolarization reserve in the presence of increased arteriogenesis, angiogenesis and connexin 43 expression in an experimental model of pacing-induced heart failure

G-CSF (granulocyte colony-stimulating factor) treatment has been shown to cause beneficial effects including a reduction of inducible arrhythmias in rodent models of ischemic cardiomyopathy. The aim of the present study was to test whether these effects do also apply to pacing-induced non-ischemic heart failure. In 24 female rabbits, heart failure was induced by rapid ventricular pacing. 24 rabbits were sham operated. The paced rabbits developed a significant decrease of ejection fraction. 11 heart failure rabbits (CHF) and 11 sham-operated (S) rabbits served as controls, whereas 13 sham (S-G-CSF) and 13 heart failure rabbits (CHF-G-CSF) were treated with 10?μg/kg G-CSF s.c. over 17?±?4?days. G-CSF treatment caused a ~25% increased arterial and capillary density and a ~60% increased connexin 43 expression in failing hearts. In isolated, Langendorff-perfused rabbit hearts eight monophasic action potential recordings showed prolongation of repolarization in CHF as compared with controls in the presence of the QT prolonging agent erythromycin (+33?±?12?ms; p?相似文献   

正常心室肌复极离散度初步研究

目的     

程序电刺激时心室复极离散度的研究

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     

Influence of biventricular pacing on myocardial dispersion of repolarization in dilated cardiomyopathy patients.

AIMS: The aim of our study was to evaluate the effect of cardiac resyncronization therapy on QT dispersion (QTd), JT dispersion (JTd), and transmural dispersion of repolarization (TDR), markers of heterogeneity of ventricular repolarization in a study population with severe heart failure. METHODS AND RESULTS: Fifty patients (43 male, 7 female, age 60.2+/-3.1 years) suffering from congestive heart failure (n=39 NYHA class III; n=11 NYHA class IV) as a result of coronary artery disease (n=19) or of dilated cardiomyopathy (n=31), with sinus rhythm (SR), QRS duration >120 ms (mean QRS duration=156+/-21 ms), an ejection fraction <35%, left ventricular end-diastolic diameter >55 mm, presence of atrioventricular asynchrony, intra- and inter-ventricular asynchrony, underwent permanent biventricular pacemaker implantation. A 12-lead standard electrocardiogram was performed at baseline, during right-, left-, and biventricular pacing (BiVP) and QTd, JTd, and TDR were assessed. BiVP significantly reduced QTd (73.93+/-19.4 ms during BiVP vs. 91+/-6.7 ms in SR, P=0.004), JTd (73.18+/-17.16 ms during BiVP vs. 100.72+/-39.04 at baseline, P=0.003), TDR (93.16+/-15.60 vs. 101.55+/-19.08 at baseline, P<0.004), compared with SR. Right ventricular endocardial pacing and left ventricular epicardial pacing both increased QTd (RVendoP 94+/-51 ms, P<0.03; LVepiP 116+/-71 ms, P<0.02), and TDR (RVendoP 108.13+/-19.94 ms, P<0.002; LVepiP 114.71+/-26.1, P<0.05). There was no effect on JTd during right and left ventricular stimulation. CONCLUSIONS: BiVP causes a statistically significant reduction of ventricular heterogeneity of repolarization and has an electrophysiological anti-arrhythmic influence on the arrhythmogenic substrate of dilated cardiomyopathy.     

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.