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Investigating Calcium-Mediated Arrhythmias via a Computational Model of a Rabbit Atrial Myocyte

机译:通过兔心房肌细胞的计算模型研究钙介导的心律失常

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The system of transverse and longitudinal sarcolemmal tubules (T-system) is observed to remodel in atrial fibrillation (AF) and heart failure (HF). The resulting calcium dysregulation has been suggested to underlie disruptions in excitation-contraction coupling, and increase the frequency of arrhythmic events at the cellular scale; however, these mechanisms and their importance are yet to be fully described. A stochastic, 3D, spatiotemporal model of the rabbit atrial myocyte was developed in order to study calcium-mediated arrhythmic phenomena at the cellular scale. Preliminary findings suggest a relationship between the severity of detubulation, and the promotion of spontaneous activity, and provides insight into the conditions required for the emergence of spontaneous activity within atrial myocytes in HF.
机译:观察到横肌和纵肌肌小管系统(T系统)在房颤(AF)和心力衰竭(HF)中重塑。已经表明,由此引起的钙失调是激发-收缩偶联破坏的基础,并在细胞规模上增加了心律失常事件的发生频率。但是,这些机制及其重要性尚未得到充分描述。为了研究钙介导的心律失常现象在细胞规模上的发展,建立了兔房性心肌细胞的随机3D时空模型。初步发现表明,在拔管的严重程度与自发活动的促进之间存在关联,并提供了对心房纤颤中自发活动出现所需条件的洞察力。

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