Vigmond E J, Leon L J
Department of Electrical & Computer Engineering, University of Calgary, Canada.
Med Biol Eng Comput. 2001 Jul;39(4):455-64. doi: 10.1007/BF02345368.
Transmural rotation of cardiac fibres can have a big influence on the initiation of re-entry in the heart. However, owing to computational demands, this has not been fully explored in a three-dimensional model of cardiac tissue that has a microscopic description of membrane currents, such as the Luo-Rudy model. Using a previously described model that is computationally fast, re-entry in three-dimensional blocks of cardiac tissue is induced by a cross-shock protocol, and the activity is examined. In the study, the effect of the transmural fibre rotation is ascertained by examining differences between a tissue block with no rotation and ones with 1, 2 and 3 degrees of rotation per fibre layer. The direction of the re-entry is significant in establishing whether or not re-entry can be induced, with clockwise re-entry being easier to initiate. Owing to the rotating anisotropy that results in preferential propagation along the fibre axis, the timing of the second stimulus in the cross-shock protocol has to be changed for different rates of fibre rotation. The fibre rotation either increases or decreases the window of opportunity for re-entry, depending on whether the activation front is perpendicular or parallel to the fibre direction. By varying the transmural extent of the S2, it is found that a deeper stimulus has to be applied to the blocks with fibre rotation to create re-entry. Increasing the transmural resistance also tends to reduce the extent of the S2 required to induce re-entry. Results suggest that increasing fibre rotation reduces the susceptibility of the tissue to re-entry, but that more complex spatiotemporal patterns are possible, e.g. stable figure-of-eight re-entries and transient rotors. Three mechanisms of re-entry annihilation are identified: front catchup, filling of the excitable gap and core wander.
心肌纤维的跨壁旋转对心脏折返的起始可能有很大影响。然而，由于计算需求，在具有膜电流微观描述的心脏组织三维模型（如Luo-Rudy模型）中尚未对此进行充分探索。使用先前描述的计算速度快的模型，通过交叉电击方案在心脏组织的三维块中诱导折返，并检查其活动。在该研究中，通过检查无旋转的组织块与每纤维层有1度、2度和3度旋转的组织块之间的差异来确定跨壁纤维旋转的影响。折返方向对于确定是否能诱导折返很重要，顺时针折返更容易起始。由于旋转各向异性导致沿纤维轴优先传播，对于不同的纤维旋转速率，交叉电击方案中第二个刺激的时间必须改变。纤维旋转根据激活前沿与纤维方向垂直或平行而增加或减少折返的机会窗口。通过改变S2的跨壁范围，发现对于有纤维旋转的组织块必须施加更深的刺激以产生折返。增加跨壁电阻也倾向于减少诱导折返所需的S2范围。结果表明，增加纤维旋转会降低组织对折返的易感性，但可能会出现更复杂的时空模式，例如稳定的8字形折返和瞬态转子。确定了三种折返消除机制：前沿追赶、可兴奋间隙填充和核心漂移。
