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首页> 外文学位 >A three-dimensional bidomain model of conduction in the ventricular wall incorporating transmural heterogeneities in action potential duration and fiber structure.
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A three-dimensional bidomain model of conduction in the ventricular wall incorporating transmural heterogeneities in action potential duration and fiber structure.

机译：心室壁传导的三维双域模型，在动作电位持续时间和纤维结构中结合了跨壁异质性。

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Intrinsic electrophysiological heterogeneity and the anisotropic muscular architecture of the ventricle conspire to form a substrate for cardiac arrhythmias. Using a computer model, we studied how these factors influence the activation and recovery processes of paced beats in the ventricle.; A section of the canine left ventricle was modeled as a three-dimensional bidomain adjoined by a blood cavity. Fenton-Karma membrane kinetics were varied transmurally to approximate the action potential duration (APD) profile observed in isolated wedges of left ventricular tissue. With uniform membrane properties, normal and premature simulated beats propagated smoothly through the tissue. However, rotational anisotropy and tissue boundaries gave rise to a complex pattern of APD caused by the misalignment of activation and recovery sequences. While the presence of intramural ionic heterogeneity did not affect the conduction of a normal epicardial beat, it establish a refractory wake that caused the subsequent premature beat to block in the midwall. Increasing electrotonic coupling across the wall reduced both APD dispersion and the extent of conduction block encountered by the premature wavefront. Although the transmural APD profile was nearly identical between epicardial and endocardial pacing, premature beats from the endocardium were not prone to block. Thus, our model shows that (1) electrophysiological heterogeneity contributes to conduction block by increasing the dispersion of refractoriness, (2) increased APD dispersion alone is an insufficient marker of functional block, and (3) decreased transmural conductivity acts to promote arrhythmia by increasing transmural APD gradients and thus the likelihood of conduction block.; To test the predictions of our computer model, we pace-mapped the canine left ventricle using 528 unipolar electrograms (UEGs) recorded simultaneously from epicardial and transmural sites. Maps of conduction velocity and activation-recovery interval (ARI) revealed (1) a tripolar pattern of ARI during normals beats that vanished in the premature beat, (2) reduced intramural conduction velocity during premature beats however, though block was not observed, and (3) while intramural ARI was longest in the midwall however, the profile was inverted following the early beat as expected from the enhanced sensitivity to diastolic interval displayed by M-cells.
机译：内在的电生理异质性和心室的各向异性肌肉结构共同形成了心律不齐的基质。使用计算机模型，我们研究了这些因素如何影响心室中节律性搏动的激活和恢复过程。犬左心室的一部分被建模为三维二维域，并与血管相连。 Fenton-Karma膜动力学通过透壁改变，以近似于在左心室组织的孤立楔形中观察到的动作电位持续时间（APD）曲线。具有均匀的膜特性，正常和过早的模拟搏动在组织中平滑传播。然而，旋转各向异性和组织边界引起了由激活和恢复序列的错位引起的APD的复杂模式。尽管壁内离子异质性的存在不影响正常心外膜搏动的传导，但它建立了难治性唤醒，导致随后的早搏在中壁受阻。跨壁的电声耦合的增加既降低了APD的色散，又降低了过早的波阵面遇到的传导阻滞的程度。尽管心外膜起搏和心内膜起搏之间的透壁APD分布几乎相同，但心内膜的过早搏动不容易被阻滞。因此，我们的模型表明（1）电生理异质性通过增加耐火度的分散性来促进传导阻滞;（2）仅APD分散性增加是功能阻滞的不足标志;（3）透壁电导率的降低通过增加心律失常而起作用透壁APD梯度，从而可能导致传导阻滞。为了测试我们的计算机模型的预测，我们使用了从心外膜和透壁部位同时记录的528个单极电描记图（UEG），对犬的左心室进行了步速映射。传导速度和激活恢复间隔（ARI）的图显示（1）在正常搏动中ARI的三极模式在早搏中消失，（2）在早搏中壁内传导速度降低，尽管未观察到阻滞，并且（3）虽然壁内ARI在中壁最长，但由于M细胞对舒张间隔的敏感性增强，因此在早期搏动后轮廓发生了反转。

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