上腺体空间密度在人类心房中的亲节律失常作用:一个in-silico研究
Karl Magtibay1, Stéphane Massé2, Kumaraswamy Nanthakumar2
1Biomedical Signal and Image Processing Laboratory, Faculty of Engineering and Architectural Science, Toronto Metropolitan University, Toronto, Ontario, Canada.
PloS one
|August 25, 2023
概括
慢性压力会导致自主功能障碍,导致心房内上腺体空间密度 (ASD) 增加. 较高的ASD水平促进了心房电生理学变化和波浪碎片化,这可能解释了年轻患者心律失常的开始.
科学领域:
- 心血管生理学心血管生理学
- 计算生物学 计算生物学
- 心脏电生理学 心脏电生理学
背景情况:
- 年轻患者 (≤45岁) 的慢性压力与自主功能障碍有关.
- 自主功能障碍表现为交感性过度活跃和在心房中的上腺刺激.
- 上腺刺激会改变心房电生理学,可能增加心律失常的易感性.
研究的目的:
- 为了研究上腺体空间密度 (ASD) 在化物中产生心律失常基质中的作用.
- 分析不同ASD水平如何影响心房电生理学和波传播.
主要方法:
- 模拟了三张25厘米2的心房板,具有不同的ASD水平,激活率和跨膜电流.
- 在50%和20% (APD50,APD20) 测量了动作潜能持续时间 (APD) 的空间和时间异质性.
- 对激发值和波面传播模式的评估影响.
主要成果:
- 越来越多的ASD缩短了APD;最大的空间异质性 (31%) 观察到15%的ASD.
- 较低的ASD (5-10%) 降低了兴奋值,而较高的ASD (>10%) 增加了它.
- 高ASD的快速激活显著增加APD50 (21%) 和APD20 (41%),改变激活时间高达120 ms.
- 高ASD促进波段分裂 (概率0.7±0.06在10%的ASD) 由于短暂的不兴奋性,与APD20空间变化相关 (ρ=0.90).
结论:
- ASD对空间和时间APD异质性以及改变的激发值有显著的贡献.
- 由于ASD引起的波浪碎片化为患有慢性压力相关的同情性过敏症的年轻患者中心律不整的开始提供了潜在的解释.
- 这项研究提供了慢性压力,自主功能障碍和心房节律失常之间的电生理学联系.
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