Local Gradients in Electrotonic Loading Modulate the Local Effective Refractory Period: Implications for Arrhythmogenesis in the Infarct Border Zone.
Local Gradients in Electrotonic Loading Modulate the Local Effective Refractory Period: Implications for Arrhythmogenesis in the Infarct Border Zone.
复制标题
DOI：
10.1109/tbme.2015.2421296
复制
发表时间：
2015-09
期刊：
影响因子：
--
通讯作者：
Bishop MJ
中科院分区：
文献类型：
--
作者：
Connolly A;Trew ML;Smaill BH;Plank G;Bishop MJ
起源于梗塞周围区域的异位电活动可引起潜在致命的折返性心律失常。梗塞边界区结构重塑导致的电紧张负荷的空间变化可能会增加局灶活动触发电捕获的可能性，但此前尚未对此进行系统研究。本研究使用计算机实验来检查有效不应期对异位搏动捕获的结构调节。根据梗塞边界区肌细胞组织的 3D 重建，快速组织扩张的区域被抽象为理想化的表示。引入了一种新颖的度量，将局部电紧张负荷定义为被动组织特性和边界条件的函数。有效不应期与局部电紧张负荷密切相关，而动作电位持续时间、传导和上冲速度在电紧张负荷增加的区域中减少。在存在局灶性异位刺激的情况下，有效不应期的空间变化可导致单向传导阻滞，为折返性心律失常提供基础。因此，根据观察到的结果，提出了一种可能的梗塞边界区心律失常发生的新机制。
Ectopic electrical activity that originates in the peri-infarct region can give rise to potentially lethal re-entrant arrhythmias. The spatial variation in electrotonic loading that results from structural remodelling in the infarct border zone may increase the probability that focal activity will trigger electrical capture, but this has not previously been investigated systematically. This study uses in-silico experiments to examine the structural modulation of effective refractory period on ectopic beat capture. Informed by 3-D reconstructions of myocyte organization in the infarct border zone, a region of rapid tissue expansion is abstracted to an idealized representation. A novel metric is introduced that defines the local electrotonic loading as a function of passive tissue properties and boundary conditions. The effective refractory period correlates closely with local electrotonic loading, while the action potential duration, conduction, and upstroke velocity reduce in regions of increasing electrotonic load. In the presence of focal ectopic stimuli, spatial variation in effective refractory period can cause unidirectional conduction block providing a substrate for reentrant arrhythmias. Consequently, based on the observed results, a possible novel mechanism for arrhythmogenesis in the infarct border zone is proposed.