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首页> 外文期刊>PACE: Pacing and clinical electrophysiology >Cycle length-associated modulation of the regional dispersion of ventricular repolarization in a canine model of long QT syndrome.
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Cycle length-associated modulation of the regional dispersion of ventricular repolarization in a canine model of long QT syndrome.

机译：长QT综合征犬模型中心室复极区域分散的周期长度相关调节。

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摘要

Previous tridimensional activation mapping showed that the development of functional conduction block at the onset of torsades de pointes was regionally heterogeneous; conduction block was frequently observed in the LV and the interventricular septum (IVS) but not in the RV, in the canine anthopleurin-A (AP-A) model of long QT syndrome (LQTS). This may be related to the distribution of myocytes with M celllike electrophysiological characteristics. To better understand the regional difference of arrhythmogenicity in LQTS, the authors investigated cycle length related modulation of ventricular repolarization among three different layers: the endocardium (End), mid-myocardium (Mid), and epicardium (Epi) of the LV and RV and at two different areas: the Epi and septum (Sep) in the IVS. The LQT3 model was produced by AP-A in dogs. Using constant pacing and single premature stimulation (S1S2), the ventricular repolarization pattern was analyzed from 256 unipolar electrograms. Activation-recovery intervals (ARIs) were used to estimate local repolarization. In seven experiments, AP-A increased regional ARI dispersion to 88.1 +/- 36.0 ms in the LV, to 72.9 +/- 35.7 ms in the IVS, and to 23.0 +/- 8.7 ms in the RV at the pacing cycle length (CL) of 1,000 ms. Development of the large ARI dispersion was due to greater ARI prolongation at the Mid site in the LV and at Sep site in the IVS. As the S1S2 interval was shortened, regional ARI dispersion decreased gradually, and finally, ARI dispersion showed a reversal gradient of repolarization between the Mid and Epi sites in the LV and between the Sep and Epi sites in the IVS. Two factors contributed to create the reversal gradient of repolarization: (1) a difference in restitution kinetics at the Mid site in the LV and at the Sep site in the IVS, characterized by a larger delta ARI and slower time constant (tau), and (2) a difference in diastolic intervals at each site resulting in different input to restitution at the same CL. However, the RV showed small alteration in the transmural dispersion of repolarization in the S1S2 protocol. S2 created heterogeneous functional conduction block in the LV and IVS but not in the RV. In the LQT3 model, the arrhythmogenicity of torsades de pointes is primarily due to dispersion of repolarization in the LV and IVS because of prominent distribution of M cells. The RV seems to participate passively in reentrant excitation during torsades de pointes.
机译：先前的三维激活图谱表明，在尖端扭转型室速发作时功能传导阻滞的发展在区域上是异质的。在长QT综合征（LQTS）的犬类花粉蛋白A（AP-A）模型中，在LV和室间隔（IVS）中经常观察到传导阻滞，而在RV中则没有观察到。这可能与具有M细胞样电生理特征的心肌细胞的分布有关。为了更好地了解LQTS的心律失常的区域差异，作者研究了三个不同层之间的周期长度相关的心室复极调节：LV和RV的心内膜（End），心中膜（Mid）和心外膜（Epi）。在两个不同的区域：IVS中的Epi和中隔（Sep）。 LQT3模型是由AP-A在犬中产生的。使用恒定的起搏和单次过早刺激（S1S2），从256个单极电描记图分析了心室复极化模式。激活恢复间隔（ARI）用于估计局部复极化。在七个实验中，在起搏周期长度下，AP-A在LV中将区域ARI色散增加到88.1 +/- 36.0毫秒，在IVS中将其增加到72.9 +/- 35.7毫秒，在RV则将其增加到23.0 +/- 8.7毫秒（ CL）为1,000毫秒。较大的ARI分散体的形成是由于LV中段和IVS的Sep位置的ARI延伸更大。随着S1S2间隔的缩短，区域ARI色散逐渐减小，最后，ARI色散在LV的中点和Epi点之间以及IVS的Sep和Epi点之间显示出反极化的反向梯度。有两个因素造成了复极的反向梯度：（1）LV中点和IVS中Sep点恢复动力学的差异，其特征在于ΔARI较大且时间常数（tau）较慢;以及（2）每个部位的舒张期间隔不同，导致在同一CL处恢复原状的输入不同。但是，RV在S1S2协议中在复极的透壁分散中显示出很小的变化。 S2在LV和IVS中产生异质功能传导阻滞，但在RV中不产生。在LQT3模型中，扭转性室性心律失常主要归因于M细胞的明显分布，从而在LV和IVS中分散了极化。右脚尖扭转期间，RV似乎被动地参与了折返激励。

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