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Effect of Transmural Differences in Excitation-Contraction Delay and Contraction Velocity on Left Ventricle Isovolumic Contraction: A Simulation Study

机译:兴奋-收缩延迟和收缩速度中透壁差异对左心室等容性收缩的影响:模拟研究

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摘要

Recent studies have shown that left ventricle (LV) exhibits considerable transmural differences in active mechanical properties induced by transmural differences in electrical activity, excitation-contraction coupling, and contractile properties of individual myocytes. It was shown that the time between electrical and mechanical activation of myocytes (electromechanical delay: EMD) decreases from subendocardium to subepicardium and, on the contrary, the myocyte shortening velocity (MSV) increases in the same direction. To investigate the physiological importance of this inhomogeneity, we developed a new finite element model of LV incorporating the observed transmural gradients in EMD and MSV. Comparative simulations with the model showed that when EMD or MSV or both were set constant across the LV wall, the LV contractility during isovolumic contraction (IVC) decreased significantly ((dp/dt)max⁡  was reduced by 2 to 38% and IVC was prolonged by 18 to 73%). This was accompanied by an increase of transmural differences in wall stress. These results suggest that the transmural differences in EMD and MSV play an important role in physiological contractility of LV by synchronising the contraction of individual layers of ventricular wall during the systole. Reduction or enhancement of these differences may therefore impair the function of LV and contribute to heart failure.
机译:最近的研究表明,左心室(LV)在电活动,激发-收缩耦合和单个心肌细胞的收缩特性的跨壁差异中引起的主动机械性能方面表现出相当大的跨壁差异。结果表明,从心内膜下层到心外膜下层,心肌细胞电激活和机械激活之间的时间(机电延迟:EMD)减少,相反,心肌细胞缩短速度(MSV)沿相同方向增加。为了研究这种不均匀性的生理重要性,我们开发了一种新的LV有限元模型,该模型结合了在EMD和MSV中观察到的透壁梯度。与该模型的比较模拟表明,当EMD或MSV或两者在LV壁上均设置为恒定时,等容收缩(IVC)期间的LV收缩性显着降低((dp / dt)max⁡降低2至38%,IVC为延长了18%至73%)。这伴随着壁应力的透壁差异的增加。这些结果表明,EMD和MSV的透壁差异通过使心室收缩过程中的心室壁各层同步同步化,对LV的生理收缩性起着重要作用。因此,减少或增强这些差异可能会损害LV的功能并导致心力衰竭。

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