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QT间期延长犬模型长间歇依赖性尖端扭转型室性心动过速机制的跨壁光学标测研究
引用本文:Liu JQ,Yang YZ,Rosenbaum DS,Laurita KR. QT间期延长犬模型长间歇依赖性尖端扭转型室性心动过速机制的跨壁光学标测研究[J]. 中华心血管病杂志, 2005, 33(6): 553-556
作者姓名:Liu JQ  Yang YZ  Rosenbaum DS  Laurita KR
作者单位:1. 116011,大连医科大学附属第一医院心脏中心
2. 美国俄亥俄克里夫兰凯斯西储大学生物医学工程系心血管研究中心
基金项目:国家留学基金,美国NIH基金HL68877(KL)赞助课题
摘    要:目的在QT间期延长(LQT)的条件下,探讨长间歇依赖性尖端扭转型室性心动过速(TdP)的电生理机制。方法同步光学标测犬左心室楔形心肌块跨壁动作电位。正常对照(n=6块),应用d-索他洛尔模拟LQT2(n=6块),应用海银花(ATX-Ⅱ)模拟LQT3(n=11块)。起搏刺激模拟长短周期现象。结果在LQT的条件下,长间歇明显延长了平均动作电位[对照组:规律刺激S1S1(291±27)ms,长间歇(307±28)ms,P>0.05;LQT2组:S1S1(356±20)ms,长间歇(381±25)ms,P<0.05;LQT3组:S1S1(609±92)ms,长间歇(675±98)ms,P<0.05]和复极化的离散[对照组:S1S1(24±6)ms,长间歇(27±6)ms,P>0·05;LQT2组:S1S1(35±9)ms,长间歇(46±11)ms,P<0.05;LQT3组:S1S1(121±85)ms,长间歇(171±98)ms,P<0.05],长间歇使M细胞的岛形分布更加明显。在LQT3组,长间歇之后更容易出现早期后除极、触发活动以及TdP(82%,P<0.05);M细胞岛的边缘是复极化阶差最大的部位,该部位也是形成单向传导阻滞和缓慢传导的部位。结论在LQT条件下,M细胞岛是TdP的发生和维持的关键部位。

关 键 词:QT间期延长 心电图 犬 动物模型 长间歇依赖性尖端扭转型室性心动过速 病理机制 跨壁光学
修稿时间:2004-10-28

Transmural optical mapping of pause dependent torsade de pointes in canine long QT models
Liu Jin-qiu,Yang Yan-zong,Rosenbaum David S,Laurita Kenneth R. Transmural optical mapping of pause dependent torsade de pointes in canine long QT models[J]. Chinese Journal of Cardiology, 2005, 33(6): 553-556
Authors:Liu Jin-qiu  Yang Yan-zong  Rosenbaum David S  Laurita Kenneth R
Affiliation:Heart Center, The First Affiliated Hospital of Dalian Medical University, Dalian 116011, China.
Abstract:OBJECTIVE: To investigate the mechanism of pause dependent torsade de pointes (TdP) in long QT (LQT) conditions. METHODS: Optical mapping was used to measure transmural action potentials from the arterially perfused left ventricular canine wedge preparation. D-sotalol and ATX-II were administered to mimic LQT 2 and LQT 3, respectively. RESULTS: In LQT models, the pause significantly enhanced M cell action potential (control group Steady state stimulation S1S1: (291 +/- 27) ms, after pause: (307 +/- 28) ms, P > 0.05; LQT 2 S1S1: (356 +/- 20) ms, after pause: (381 +/- 25) ms, P < 0.05; LQT 3 S1S1: (609 +/- 92) ms, after pause: (675 +/- 98) ms P < 0.05), dispersion of transmural repolarization (control group S1S1: (24 +/- 6) ms, after pause: (27 +/- 6) ms, P > 0.05; LQT 2 S1S1: (35 +/- 9) ms, after pause: (46 +/- 11) ms, P < 0.05; LQT 3 S1S1: (121 +/- 85) ms, after pause: (171 +/- 98) ms, P < 0.05) and the M cell island-like distribution more clearly compared to baseline pacing. Pause dependent early afterdepolarizations (EADs), EAD-induced triggered activity and TdP more likely occurred under LQT 3 condition (82%, P < 0.05). The triggered beat after pause often broke through at the margin of M cells island where the repolarization gradients was maximal. The unidirectional conduction block and slow conduction were observed vividly at this region. CONCLUSION: These data suggest that M cells island plays an important role in origination and maintenance of pause dependent TdP.
Keywords:Long QT syndrome  Tachycardia  ventricular  Electrophysiology
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