自主神经系统对在体犬跨室壁复极不均一性影响的研究

目的　探讨自主神经系统对在体犬跨室壁复极离散度的影响。方法　用单相动作电位(MAP)记录技术 ,同步记录 12只开胸犬左心室游离壁心外膜心肌 (epicardium ,Epi)、中层心肌(midmyocardium ,Mid)和心内膜心肌 (endocardium ,Endo)的MAP。对自主神经刺激前和刺激过程中 ,三层心肌的跨室壁复极离散度和早期后除极的发生率进行比较。结果　起搏周长为 10 0 0ms时 ,在未刺激自主神经的情况下 ,Epi、Mid和Endo的单相动作电位时程 (MAPD)复极 90 %的时限 (MAPD90 )分别是 (2 78± 11)ms、(316± 16 )ms和 (2 70± 12 )ms;其中Mid的MAPD90 明显长于Epi和Endo的MAPD90 (P<0 0 1)。刺激交感神经时 ,Epi、Mid和Endo细胞的MAPD90 分别缩短 (19± 4 )ms、(45± 6 )ms、(18± 3)ms。与刺激前相比 ,跨室壁复极离散度由 (44± 4 )ms减少到 (15± 3)ms(P <0 0 1) ;但是交感神经刺激时 ,有 5只犬 (41% )的中层心肌出现了早期后除极。迷走神经刺激对三层心肌的MAPD90 值无明显影响。结论　 (1)在体犬心室肌存在跨室壁复极不均一性 ;(2 )交感神经刺激可减少跨室壁复极离散度 ,但易在Mid诱发早期后除极 ;(3)迷走神经刺激对跨室壁复极离散度无明显影响。     

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.     

跨室壁复极离散与恶性室性心律失常

目的探讨恶性室性心律失常病人的跨室壁复极离散度。方法恶性室性心律失常组11例,健康对照组13例,对两组的跨度壁复极离散度分别进行测量。结果恶性室性心律失常组病人的跨室壁复极离散度明显大于健康对照组(P<0.01),差异有统计学意义。结论跨室壁复极离散增大可能是发生恶性室性心律失常的预测指标之一。     

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。     

急性缺血对兔左心室跨壁复极离散度的影响

急性缺血是导致室性心律失常、心脏性猝死的主要原因之一。本研究以经冠状动脉灌注的兔左心室楔形心肌组织块为对象，着重探讨了急性无灌注缺血过程中兔左心室内外膜心肌动作电位、跨壁复极离散度（transmural dispersion of repolarization，TDR）演变规律及室性心律失常发生机制。     

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。     

犬在体心肌跨室壁复极不均一性的研究

目的　探讨犬在体心肌是否存在跨室壁复极不均一性。方法　用单相动作电位记录技术 ,同步记录 10只开胸犬在体心脏正常及心率减慢状态下心外膜心肌 (epicardium ,Epi)、中层心肌(midmyocardium ,Mid)及心内膜心肌 (endocardium ,Endo)单相动作电位 (monophasicactionpotential,MAP) ,测量单相动作电位时程 (MAPD)并比较其差异。结果　在心动周期 30 0ms时 ,Epi、Mid及Endo的MAP复极化达到 90 %的单相动作电位时程 (MAPD90 )分别为 (2 0 8 6 7± 44 37)ms、(2 0 9 17± 38 6 2 )ms、(2 0 3 5 0± 33 84)ms,在体三层心肌MAPD无明显差异 ;心动周期增加至 2 0 0 0ms时 ,三层心肌MAPD呈慢频率依赖性延长 ,Epi、Mid及Endo的MAPD90 分别为 (32 9 90± 31 90 )ms、(36 9 90± 35 0 9)ms、(317 2 0± 40 2 7)ms,其中Mid的MAPD90 延长最为显著 ,与Epi及Endo相比 ,差异有显著性 (P <0 0 5 )。结论　犬在体心肌存在明显慢频率依赖性的跨室壁复极不均一性 ,而Mid细胞的电生理特征可能是导致这一差异的基础。     

左室壁中层心肌起搏对缺血再灌注犬跨室壁复极离散的影响

目的研究心室壁中层(M层)起搏对缺血再灌注犬跨壁复极离散(TDR)的影响,探讨采用M层起搏技术防治TDR增大相关性心律失常的可行性。方法制作正常犬及缺血再灌注后犬左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程(APD)及TDR的变化。结果心室内、外膜和M层起搏,心肌各层APD无显著变化(P﹥0.05);在正常状态时,心外膜起搏时,心外膜与M层之间的传导时间(TM-Epi)(24.3±2.4ms)显著长于心内膜起搏(12.0±0.8 ms)或M层起搏(12.6±0.7 ms)时的TM-Epi(P﹤0.05)。M层起搏时,TDR较外膜起搏明显减小(34.9±5.4 ms vs 71.5±6.1 ms,P﹤0.01),与内膜起搏(35.9±5.4 ms)相比无显著差异(P﹥0.05)。缺血再灌注后,结果与正常状态时相似。心外膜起搏(32.3±5.8 ms)时,TM-Epi较M层起搏(15.1±2.9ms)或内膜起搏(15.3±2.8 ms)进一步延长(P﹤0.05)。M层起搏时,TDR较外膜起搏明显减小(63.3±13.3 msvs 111.1±17.7 ms,P﹤0.01),与内膜起搏(62.8±13.8 ms)相比无显著差异(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,无明显差别。     

胺碘酮对家兔急性心肌缺血左室跨壁复极离散度的影响

目的:探讨胺碘酮对家兔急性缺血左室心肌楔形组织块电生理特性和跨壁复极离散度（TDR）的影响及其抗缺血心律失常的机制。方法: 建立冠状小动脉灌注家兔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时,胺碘酮对内外层心肌细胞的动作电位时程（APD）、TDR和心律失常的影响。结果: ①左心室楔形组织块停止灌注后,胺碘酮组内、外膜心肌细胞的APD较对照组明显延长[(228±19) ms vs.(212±6) ms,P<0.05］,且外膜APD的延长更明显[(203±15) ms vs.(180±5) ms,P<0.05］。②急性缺血各时间段,APD较缺血前均缩短,以外膜APD缩短更明显,导致TDR增大。用药后TDR明显短于对照组。结论: 胺碘酮可延长内、外膜心肌细胞的APD,且外膜APD的延长明显,并可减小急性缺血心肌的TDR,这可能是其抗心律失常机制的细胞电生理基础。     

Azimilide对犬三层心肌细胞动作电位时程及跨壁复极离散度的影响

目的探讨抗心律失常药物Azimilide对犬三层心肌细胞动作电位时程(APD)及跨壁复极离散度(TDR)的影响。方法建立冠状动脉灌注的犬左室心肌组织块模型,观察不同浓度的Azimilide(0.3,10,30μmol/L)灌流对内、中、外三层细胞APD、TDR及早期后除极(EAD)的作用,及是否诱发尖端扭转型室性心动过速(Tdp)。结果Azimilide延长三层细胞的APD,尤以心外膜细胞最为明显,因而减小TDR;Azimilide延长APD与剂量呈非线性效应,30μmol/L延长三层心肌细胞的APD90不如10μmol/L延长明显;Azimilide可在心外膜诱发EAD及室性早搏(6个模型中有3个模型诱发),但未诱发出Tdp。结论 Azimilide延长复极时间但不增加TDR,具有较小的致心律失常效应。     

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     

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。     

Comparison of ECG Variables of Dispersion of Ventricular Repolarization with Direct Myocardial Repolarization Measurements in the Human Heart

Validation of ECG Variables of Dispersion. Introduction: QT dispersion (QTD) from the 12-tead ECG has been widely adopted as a noninvasive index of dispersion of ventricular repolarization (DVR). QTD, however, has never been validated by direct comparison with myocardial DVR in the human heart. Methods and Results: Monophasic action potential (MAP) recordings obtained in an earlier study were retrospectively matched with 12-lead ECGs available from within 24 hours of the invasive procedure. MAPs were available from an average of 8 ± 3 left endocardial sites in 4 patients with left ventricular hypertrophy (LVH) and 7 patients with normal ECGs, and 6 ± 2 epicardial sites in 3 patients of each group during normal ventricular activation. Local repolarization time (RT) was determined as MAP duration at 90% repolarization plus the local activation time. Dispersion of RT was calculated as the difference between the earliest and latest RT. ECGs were digitized and analyzed with recently described interactive QTD analysis software. In addition to standard QTD (defined as QT_max– QT_min), all currently proposed ECG dispersion variables were compared and correlated with the invasive measurements of DVR. QTD exhibited a reasonable correlation with dispersion of RT (R = 0.67; P < 0.01). Several other variables designed to measure DVR exhibited a similar, but not better, correlation. Among them, the QT peak/QT end ratio in V₃ (R =?0.72; P < 0.01) and averaged over all analyzableleads (R =?0.59; P < 0.01) exhibited a good correlation with dispersion of RT, which was further improved when endocardial measurements were considered alone. T area measures did not correlate with dispersion of RT, but discriminated LVH. Conclusion: DVR can he assessed by means of a 12-lead surface ECG. Several of the variables under study exhibit a similar accuracy in determination of true myocardial dispersion of repolarization. Variables involving the terminal part of repolarization, such as the QT peak/QT ratio, even from a single lead, may add to the determination of DVR from the human heart.     

心室跨壁复极离散度预测心脏再同步治疗除颤器术后快速室性心律失常的风险

目的：心脏再同步治疗除颤器（CRT-D）增加了心室复极离散度（TDR）,本研究旨在评价心肌跨壁复极离散度指标中的QTc间期,T波顶点（T p）T波终点（Te）之间的时限（TpTe）和TpTe /QTc是否与CRT-D患者需治疗的快速室性心律失常相关。方法：2011-01至2013-01连续选取160例于我院行CRT-D植入的患者,所选资料为术后即刻心电图,分析其V5导联的QTc间期,TpTe,TpTe/QTc值以评估其TDR,所有植入CRT-D患者均于我中心常规随访,随访时间为（20±10）个月。快速室性心律失常的发生均采自程控仪调取的CRT-D记录。结果：其中因持续性室性心动过速、心室颤动接受CRT-D治疗的患者为30例（治疗组,18.7%）,未治疗的患者为未治疗组（130例,81.3%）。治疗组的TpTe/QTc (0.24±0.05 vs 0.20±0.04,P<0.001)和 TpTe [(119±30) ms vs (95±20) ms,P<0.001]较未治疗组明显增加,但两组间QTc间期差异无统计学意义[（480±60）ms vs (470±70) ms,P=0.6]。QTc间期与CRT-D治疗的风险无相关性。TpTe/QTc ≥0.25预测CRT-D患者室性心律失常风险的敏感性和特异性分别为47%和91%,而TpTe≥120 ms预测CRT-D患者室性心律失常风险的敏感性和特异性分别为40%和95%。CRT-D术后患者生存曲线分析表明,TpTe/QTc和TpTe均能有效预测患者的预后情况（P<0.001）。结论：TpTe和TpTe/QTc 的增加显著增加再同步治疗除颤器患者术后需CRT-D治疗的风险。     

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。     

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.     

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.     

Dispersion of atrial repolarization in patients with paroxysmal atrial fibrillation.

To study the role of the dispersion of atrial repolarization (DAR) in the genesis of atrial fibrillation (AF), monophasic action potentials (MAP) were recorded simultaneously from a catheter at the high lateral right atrium (HLRA) and a catheter moving around the high, middle and low lateral right atrium (RA) the high, anterior and posterior septal RA and the RA appendage in 15 patients with paroxysmal AF and 15 patients with atrioventricular nodal re-entry tachycardia (AVNRT) or concealed Wolff-Parkinson-White syndrome (WPW) without history of AF. After recordings during sinus rhythm (SR), MAPs were recorded during programmed stimulation (PS) via the HLRA catheter at a drive cycle length (CL) of 500 ms. Thus, MAPs were recorded simultaneously from 2 sites at a time and sequentially from 4 to 12 sites during SR, drive pacing and PS. Taking the MAP at the HLRA as reference, the dispersion of repolarization time (dispersion of RT) and its two components, the dispersions of activation time (dispersion of AT) and MAP duration (dispersion of MAP duration) among the 4 to 12 sites were calculated and taken as parameters of DAR. RESULTS: During SR and PS, the maximal dispersion of RT was significantly greater in AF than in control patients, 113+/-49 ms vs 50+/-28 ms (P<0.001) and 114+/-56 vs 70+/-43 ms (P<0.05) respectively. The increased dispersion of RT in the AF group was caused by increases in both dispersion of MAP duration and dispersion of AT. CONCLUSION: During SR and PS, DAR increased in patients with paroxysmal AF due to increases in dispersion of MAP duration and dispersion of AT, which suggests the involvement of both repolarization and conduction disturbances in the development of paroxysmal AF.     

Transmural dispersion of repolarization and ventricular tachyarrhythmias

BACKGROUND: Myocardial transmural dispersion of repolarization (TDR) has been associated with reentrant arrhythmias in animal studies but a clinical association has not yet to been demonstrated. The present study examines the relationship between TDR and ventricular tachyarrhythmias in human subjects. METHODS: This study consisted of 65 patients with non-sustained ventricular tachycardia, sustained ventricular tachycardia, ventricular fibrillation or unexplained syncope with organic heart disease. The control group included 65 patients with paroxysmal supraventricular tachycardia. The 12 ECG was recorded at a recording rate of 100 mm/sec. The interval from the peak to the end of the T wave in the precordial (ECG), referred to as TpTe was assumed to be representative of TDR. RESULTS: Patients were divided into three groups based on the ability to induce VT at the time of electrophysiologic study: VT inducible group (n=37), VT non-inducible group (n=25) and control group (n=65). V4 TpTe/ radical RR was significantly prolonged in the VT inducible group, as compared to the VT non-inducible group (n=25) and the control group (118.9 +/- 26.1 vs. 103.9 +/- 25.7, 104.1 +/- 22.6 ms, P<.05). Patients who develop VT spontaneously (n=13) during a mean follow-up period of 25 months, displayed significantly prolonged V3 TpTe/ radical RR, compared to patients who did not develop VT spontaneously or the control group (132.5 +/- 37.4 vs. 109.8 +/- 26.3, 107.1 +/- 24.1 ms, P <.05). CONCLUSION: Prolonged TDR is associated with inducibility as well as spontaneous development of VT in higher risk patients. TDR may be a useful index for predicting ventricular tachyarrhythmias.     

兔LQT2模型时空复极异质性变化与室性心律失常发生的关系

为探讨心室跨壁复极离散度(TDR)和动作电位时程(APD)恢复性质的变化在LQT2室性心律失常发生中的作用,笔者采用冠状动脉灌注的兔左室肌楔形组织块制备LQT2模型。标本随机分四组:对照组(标准台氏液灌注);LQT2模型(简称模型)组(100μmol/Ld,l-sotalol灌流);模型+低钾(3mmol/L)组和模型+低钾+维拉帕米(2μmol/L)组。观察不同基础周长(BCL)刺激(500,1000和2000ms)条件下,四组标本APD90、TDR和APD恢复性质的变化与室性心律失常发生的关系。结果:①在不同BCL条件下,与对照组相比,模型组、模型+低钾组及模型+低钾+维拉帕米组的内外膜心肌细胞的APD90均增大,以内膜心肌细胞的APD90增大显著,导致TDR增加。②BCL为500和1000ms时,与对照组相比,模型组、模型+低钾组的APD恢复曲线斜率显著增加,而模型+低钾+维拉帕米组,差异无显著性。③在BCL为1000和2000ms时,给予S1S2程序刺激,模型+低钾组尖端扭转性室性心动过速发生率为5/7。结论:TDR增大和APD恢复性质的变化在室性心律失常的发生中均起着重要的作用。