Microfibrosis produces electrical load variations due to loss of side-to-side cell connections: A major mechanism of structural heart disease arrhythmias
Microfibrosis produces electrical load variations due to loss of side-to-side cell connections: A major mechanism of structural heart disease arrhythmias
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DOI：
10.1111/j.1540-8159.1997.tb06199.x
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发表时间：
1997-02-01
影响因子：
1.8
通讯作者：
Boineau, JP
中科院分区：
文献类型：
--
作者：
Spach, MS;Boineau, JP
本文的目的是证明心肌微结构的适应性变化如何为引发折返性心律失常的新的传导障碍提供机制。这些机制是基于细胞负荷增加所产生的不连续传导现象;这些增加是由差距连接的正态分布变化引起的。最近的研究表明，在微观水平上，正常成熟心肌中的传播是随机的。例如，这种正常肌肉中的差距连接的不均匀和不规则分布产生与纵向和横向传播期间单个细胞内的V对点（max）的变化相关联的负荷变化。在微观水平上正常传播的随机性通过在兴奋事件发生小变化后重建波前运动的一般趋势提供了相当大的保护，以防止心律失常。如果这样的微观多样性降低，负载的大的波动发展，分布在比平常更多的小区。多样性的减少可能是由于纤维之间的侧对侧耦合的损失引起的，这产生了具有微纤维化的相对孤立的细胞群。随着侧到侧光纤耦合的损失，心肌结构可能无法在宏观水平上重建平滑的波前。电负载的空间不均匀性则引起传导阻滞和折返。
The purpose of this article is to demonstrate how adaptive changes in myocardial microstructure provide mechanisms for emergent new conduction disturbances that initiate reentrant arrhythmias. The mechanisms are based on discontinuous conduction phenomena produced by increases in cellular loading; these increases result from changes in the normal distribution of the gap junctions. Recent studies indicate that at a microscopic level propagation in normal mature cardiac muscle is stochastic. For example, the nonuniform and irregular distribution of the gap junctions in such normal muscle produces load variations that are associated with changes in V over dot(max) inside individual cells during both longitudinal and transverse propagation. The stochastic nature of normal propagation at a microscopic level offers considerable protection against arrhythmias by reestablishing the general trend of wavefront movement after small variations in excitation events occur. If such microscopic diversity is decreased, large fluctuations in load develop that are distributed over more cells than usual. The decrease in diversity may be caused by loss of side-to-side coupling between fibers, which produces relatively isolated groups of cells with microfibrosis. With loss of side-to-side fiber coupling, the myocardial architecture may fail to reestablish a smoothed wavefront at the macroscopic level. Spatial nonuniformities of electrical loading then give rise to conduction block and reentry.