Three Distinct Directions of Intramural Activation Reveal Nonuniform Side-to-Side Electrical Coupling of Ventricular Myocytes
Three Distinct Directions of Intramural Activation Reveal Nonuniform Side-to-Side Electrical Coupling of Ventricular Myocytes
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DOI：
10.1161/circep.108.830133
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发表时间：
2009-08-01
影响因子：
8.4
通讯作者：
Smaill, Bruce H.
中科院分区：
文献类型：
--
作者：
Caldwell, Bryan J.;Trew, Mark L.;Smaill, Bruce H.
背景-心脏组织的各向异性是心脏中 3D 电传播和激活波前稳定性的关键决定因素。心室心肌的电特性被广泛认为是轴向各向异性的，激活在肌纤维方向上传播最快，并且以横向于该方向的均匀速度传播。我们提出了与这一观点相矛盾的新实验证据。方法和结果-首次使用来自猪左心室组织的高密度壁内电测绘（325 个电极，间距约为 4x4x1 毫米）来重建 3D 起搏激活表面，直接投影到在整个相同左心室体积中成像的 3D 组织结构上。来自 5 颗心脏的这些数据表明，心室组织是电正交各向异性的，具有 3 个不同的传播方向，这些方向与心室肌细胞层状排列定义的局部微结构轴一致。 0.67 +/- 0.019 ms(-1) 的最大传导速度与肌纤维轴对齐。然而，与此相反，最大传导速度为 0.30 +/- 0.010 ms(-1)，平行于肌细胞层，0.17 +/- 0.004 ms(-1) 垂直于肌细胞层。这些正交各向异性传导速度产生了穿过左心室游离壁的优先激活路径，这些路径未被结构详细的计算机模型捕获，该模型包含轴向各向异性电特性。结论——我们的研究结果表明，当前关于心脏中均匀侧对侧电耦合的观点需要修改。特别是，不均匀的层状心肌结构和相关的电各向异性应包含在室性心律失常的启动和维持的未来模型中。 （循环心律失常电生理学。2009；2：433-440。）
Background-The anisotropy of cardiac tissue is a key determinant of 3D electric propagation and the stability of activation wave fronts in the heart. The electric properties of ventricular myocardium are widely assumed to be axially anisotropic, with activation propagating most rapidly in the myofiber direction and at uniform velocity transverse to this. We present new experimental evidence that contradicts this view.Methods and Results-For the first time, high-density intramural electric mapping (325 electrodes at approximate to 4x4x1-mm spacing) from pig left ventricular tissue was used to reconstruct 3D paced activation surfaces projected directly onto 3D tissue structure imaged throughout the same left ventricular volume. These data from 5 hearts demonstrate that ventricular tissue is electrically orthotropic with 3 distinct propagation directions that coincide with local microstructural axes defined by the laminar arrangement of ventricular myocytes. The maximum conduction velocity of 0.67 +/- 0.019 ms(-1) was aligned with the myofiber axis. However, transverse to this, the maximum conduction velocity was 0.30 +/- 0.010 ms(-1), parallel to the myocyte layers and 0.17 +/- 0.004 ms(-1) normal to them. These orthotropic conduction velocities give rise to preferential activation pathways across the left ventricular free wall that are not captured by structurally detailed computer models, which incorporate axially anisotropic electric properties.Conclusions-Our findings suggest that current views on uniform side-to-side electric coupling in the heart need to be revised. In particular, nonuniform laminar myocardial architecture and associated electric orthotropy should be included in future models of initiation and maintenance of ventricular arrhythmia. (Circ Arrhythmia Electrophysiol. 2009;2:433-440.)