Laminar arrangement of ventricular myocytes influences electrical behavior of the heart
Laminar arrangement of ventricular myocytes influences electrical behavior of the heart
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DOI：
10.1161/circresaha.107.161075
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发表时间：
2007-11-09
影响因子：
20.1
通讯作者：
Smaill, Bruce H.
中科院分区：
文献类型：
--
作者：
Hooks, Darren A.;Trew, Mark L.;Smaill, Bruce H.
心脏对电击的反应、窦性心律中的电传播以及心室颤动的时空动力学都严重依赖于心脏组织的电各向异性。长期以来，人们对心脏电各向异性的看法是，沿着肌细胞轴的电导率最大，这使得电激活在这个方向上的传播速度最快，并且电导率在肌细胞轴的横向上是各向同性的，支持在这个平面上较慢的均匀传播。在这种情况下，了解与肌纤维轴平行和横向的两个方向的电导率，足以表征心脏的电作用。在这里，我们提出了新的实验数据来挑战这一观点。我们使用了一种新颖的结合内部电测绘和实验特定的计算机建模的方法，来证明左心室心肌具有与三个微观结构定义的轴相关的独特的体积电导率。结果表明，肌内电流注入产生的电压场不仅受肌纤维方向的影响，还受肌层或肌层的跨壁排列的影响。在这些实验的计算机模型中，测量的三维组织结构被硅重建，记录的电压与肌纤维方向的电导率最匹配，平行于肌层和垂直于肌层的电导率分别为4:2:1。这些发现将心脏组织重新定义为电正交异性基质，并增强了我们对外部电击如何成功地将颤动的心脏重置为均匀电状态的理解。更一般地说，控制协调电传播不稳定到室性心律失常的机制需要根据这一发现进行评估。
The response of the heart to electrical shock, electrical propagation in sinus rhythm, and the spatiotemporal dynamics of ventricular fibrillation all depend critically on the electrical anisotropy of cardiac tissue. A long-held view of cardiac electrical anisotropy is that electrical conductivity is greatest along the myocyte axis allowing most rapid propagation of electrical activation in this direction, and that conductivity is isotropic transverse to the myocyte axis supporting a slower uniform spread of activation in this plane. In this context, knowledge of conductivity in two directions, parallel and transverse to the myofiber axis, is sufficient to characterize the electrical action of the heart. Here we present new experimental data that challenge this view. We have used a novel combination of intramural electrical mapping, and experiment-specific computer modeling, to demonstrate that left ventricular myocardium has unique bulk conductivities associated with three microstructurally-defined axes. We show that voltage fields induced by intramural current injection are influenced by not only myofiber direction, but also the transmural arrangement of muscle layers or myolaminae. Computer models of these experiments, in which measured 3D tissue structure was reconstructed in-silico, best matched recorded voltages with conductivities in the myofiber direction, and parallel and normal to myolaminae, set in the ratio 4:2:1, respectively. These findings redefine cardiac tissue as an electrically orthotropic substrate and enhance our understanding of how external shocks may act to successfully reset the fibrillating heart into a uniform electrical state. More generally, the mechanisms governing the destabilization of coordinated electrical propagation into ventricular arrhythmia need to be evaluated in the light of this discovery.