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Effect of Heart Failure-induced Electrical Remodeling on the Initiation of Atrial Arrhythmias

机译:心力衰竭诱导的电气重塑对心理心律失常引发的影响

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Heart failure (HF) is a particularly prevalent clinical condition promoting atrial arrhythmias. However, the underlying mechanism is rarely studied. In this study, using a GPU-based simulation, a biophysically detailed computational model of the three-dimensional (3D) sheep atria was implemented to investigate the mechanism by which HF-induced electrical remodeling promoting atrial arrhythmia. At both the single cell and the 3D levels of the sheep atrial model, effects of such HF-induced electrical remodeling on the electrical properties were evaluated. At the cellular level, simulation results demonstrated that the action potential duration (APD) and the amplitude of systolic Ca~(2+) transient were decreased in all cell types except the PV cell in the HF condition. At the 3D whole organ level, simulation results showed that though localized APDs were shortened, the spatial electrical heterogeneity was maintained in the HF condition, resulting in an increased vulnerability of the tissue for the initiation of the conduction block in response to a premature stimulus. This study provided new insights into understanding the mechanism by which HF promoted atrial arrhythmias.
机译:心脏衰竭(HF)是一个特别普遍的临床病症促进房性心律失常。但是,基本的机制研究很少。在这项研究中,采用了基于GPU的仿真,三维(3D)羊心房的生物物理学详细计算模型的实施是为了调查由HF诱导电重构促进房性心律失常的机制。在单细胞和3D水平羊心房模型的两者上的电性能,例如HF诱导电重构的效果进行了评价。在细胞水平上,模拟结果表明,动作电位持续时间(APD)和收缩的Ca〜(2+)瞬变的幅度在所有细胞类型均下降,除了在HF条件的PV电池。在3D整个器官水平,模拟结果表明,虽然局部APD的被缩短,空间电异质性保持在HF条件,从而导致组织的传导阻滞的发起响应于过早刺激的增加的脆弱性。这项研究提供了新的见解理解由HF促进房性心律失常的机制。

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