Department of Biomedical Engineering, City College of New York, City University of New York, New York, USA.
Med Biol Eng Comput. 2012 Aug;50(8):813-25. doi: 10.1007/s11517-012-0934-4. Epub 2012 Jun 23.
Cardiac arrhythmias are initiated in regions that undergo cellular remodeling as a result of disease. Using a sub-cellular model of myocardium, we studied the mechanism of block caused by tissue microstructure remodeling: cell geometry [quantified as length/width (L/W) cell ratio] and cell-to-cell coupling (G(j)). Heterogeneities in cell L/W ratio and G ( j ) lead to block when excitability is reduced and the corresponding space constant λ (in the direction of propagation) increases by >40 %. Tissue architectures with elongated cells (i.e. large cell L/W ratios) that are better coupled (i.e. large G(j)) are less prone to block at sites of regional heterogeneities in cell geometry and/or cell coupling than tissue architectures consisting of cells with smaller L/W ratios and/or poorer coupling. Whether an increase in tissue anisotropic ratio (ANR) is arrhythmogenic or not depends on the cellular mechanism of the increase: ANR leads to an increased risk of block when G(j) decreases, but to a decreased risk of block when cell L/W ratio increases. Our findings are useful to understand the mechanisms of block in cardiac pathologies that result in tissue architecture remodeling.
心律失常是由疾病引起的细胞重构区域引发的。我们使用心肌的亚细胞模型研究了组织微观结构重构引起的阻滞机制：细胞几何形状[用长度/宽度（L/W）细胞比量化]和细胞间耦合（G（j））。当兴奋性降低并且相应的空间常数 λ（在传播方向上）增加超过 40%时，细胞 L/W 比和 G（j）的异质性导致阻滞。与由具有较小 L/W 比和/或较差耦合的细胞组成的组织结构相比，具有长形细胞（即大细胞 L/W 比）和更好耦合（即大 G（j））的组织结构在细胞几何形状和/或细胞耦合的区域异质性部位更不容易发生阻滞。组织各向异性比（ANR）的增加是否有致心律失常作用取决于增加的细胞机制：当 G（j）降低时，ANR 导致阻滞的风险增加，但当细胞 L/W 比增加时，阻滞的风险降低。我们的发现有助于理解导致组织重构的心脏病理学中的阻滞机制。
