Effects of early afterdepolarizations on reentry in cardiac tissue: a simulation study
Effects of early afterdepolarizations on reentry in cardiac tissue: a simulation study
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DOI：
10.1152/ajpheart.01309.2006
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发表时间：
2007-06-01
影响因子：
4.8
通讯作者：
Kogan, Boris
中科院分区：
文献类型：
--
作者：
Huffaker, Ray B.;Weiss, James N.;Kogan, Boris
早期后除极(EAD)通常是在心率缓慢时产生的，此时复极储备因遗传性疾病或药物而减少。然而，如果复极储备充分减少，EADS托盘也会以快速心率出现。在这种情况下，舒张期肌浆网(SR)自发的钙释放可以通过增加动作电位平台期间的内向电流来促进细胞EAD的形成。允许重新激活窗口L型钙电流以逆转复极化。这里。我们研究了自发性SR-Ca释放引起的EADS或折射波在模拟的One-Ea中传播的影响。两个人。并使用三维均质心脏组织，一个版本的Luo-Rudy动态心室动作电位模型进行了修改，以增加这些EAD的可能性。我们发现：1)在再入过程中。自发性肌浆网钙释放的不均匀与整个组织的兴奋历史的细微差异有关，这些组织产生了有和没有EADS的相邻区域。这使得EAD能够启动新的波前传播到复极化组织中：2)EAD-Lenerated波前。EADS可沿原始或相反方向传播，作为单个新波或两个新波，依赖于油和与EAD区域接壤的组织的耐火性-3)通过突然延长局部不应性，EADS引起快速转子位移，移位电轴：4)快速转子位移通过与组织边界碰撞促进自终止，但持续的EADS可再生单一或多个焦点激发，从而重新启动重返大气层。这些发现可能解释了尖端扭矩的许多特征。例如由焦点激发、快速变化的电轴引起的永久化。经常自我终止，偶尔退化为纤颤。
Early afterdepolarizations (EADs) are classically generated at slow heart rates when repolarization reserve is reduced by genetic diseases or drugs. However, EADs tray also occur at rapid heart rates if repolarization reserve is Sufficiently reduced. In this setting, spontaneous diastolic sarcoplasmic reticulum (SR) Ca release can facilitate cellular EAD formation by augmenting inward Currents during the action potential plateau. allowing reactivation of the window L-type Ca Current to reverse repolarization. Here. we investigated the effects of spontaneous SR Ca release-induced EADs or, reentrant wave propagation in simulated one-. two-. and three-dimensional homogeneous cardiac tissue using, a version of the Luo-Rudy dynamic ventricular action potential model modified to increase the likelihood of these EADs. We found: 1) during reentry. nonuniformity in spontaneous SR Ca release related to subtle differences in excitation history throughout the tissue created adjacent regions with and Without EADs. This allowed EADs to initiate new wavefronts propagating into repolarized tissue: 2) EAD-Lenerated wavefront. Could propagate ill either the original or opposite direction, as a single new wave or two new waves, depending oil the refractoriness of tissue bordering the EAD region-3) by suddenly prolonging local refractoriness, EADs caused rapid rotor displacement, shifting the electrical axis: and 4) rapid rotor displacement promoted self-termination by collision with tissue borders, but persistent EADs Could regenerate single Or Multiple focal excitations that reinitiated reentry. These findings may explain many features of Torsades des pointes. such as perpetuation by focal excitations, rapidly changing electrical axis. frequent self-termination, and occasional degeneration to fibrillation.