左心室几何形状改变左心室动脉瘤实验模型边界区应力时间分布:有限元模型研究

P. Moustakidis, H. Maniar, B. Cupps, T. Absi, Jie Zheng, J. Guccione, T. Sundt, M. Pasque
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引用次数: 45

摘要

背景:左心室动脉瘤(LVA)是心肌梗死的重要并发症,可导致整体左心室功能障碍。然而,这种异常功能的确切机制尚未阐明。在这项研究中,我们检验了左心室几何形状的变化导致心室壁应力增加和左心室边界区(BZ)应力时间分布变化的假设。方法在成年多塞特羊(n=8)中建立经壁根尖前梗死,并使其成熟为lva 10周。随后使用MRI对动物进行成像,同时记录脑室内压力。利用心脏舒张末期、等容收缩期、收缩期峰值和收缩期末期的MRI图像构建心脏模型。分析了2个短轴切片,1个基部和1个顶端。顶端切片包括动脉瘤的间隔部分和前部分,以及相应的bz和正常心肌。采用有限元分析计算区域壁面应力,并与正常对照羊相应区域的应力进行比较(n=7)。结果LVA组舒张末期、等容期、收缩期高峰、收缩期末期BZ压力均显著升高(P <0.001)。此外,应力的时间分布也发生了显著变化,最大应力出现在峰值而不是等容收缩期。结论左左心室的几何变化增加了壁应力,改变了壁应力在BZ区的时间分布。这一发现与相应的区域血流量、耗氧量和机械收缩性能的相关性可能有助于阐明所观察到的全局左室功能障碍的机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Altered Left Ventricular Geometry Changes the Border Zone Temporal Distribution of Stress in an Experimental Model of Left Ventricular Aneurysm: A Finite Element Model Study
BackgroundLeft ventricular aneurysm (LVA) is a significant complication of myocardial infarction that may lead to global left ventricular (LV) dysfunction. However, the exact mechanism underlying the abnormal function has not been elucidated. In this study we tested the hypothesis that changes in LV geometry cause both an increase in wall stress and a change in the temporal distribution of stress in the LVA border zone (BZ) during systole. MethodsTransmural anteroapical infarcts were created in adult Dorsett sheep (n=8) and were allowed to mature into LVAs for 10 weeks. Animals were imaged subsequently using MRI with simultaneous recording of intraventricular pressures. Cardiac models were constructed from the MRI images at end-diastole, isovolumic systole, peak-systole and end-systole. Two short-axis slices, 1 basal and 1 apical were analyzed. The apical slice included the septal and anterior component of the aneurysm as well as the corresponding BZs and normal myocardium. Regional wall stresses were calculated using finite element analysis and compared with stresses in corresponding regions from normal control sheep (n=7). ResultsIn the LVA group, stress was significantly increased in the BZ at the end-diastolic, isovolumic, peak-systolic, and end-systolic instants (P <0.001 for all). In addition the temporal distribution of stress was significantly altered with maximum stress occurring at peak instead of isovolumic systole. ConclusionsGeometric changes in the LVA hearts increased wall stress and altered its temporal distribution in the BZ region. Correlation of this finding with the corresponding regional blood flow, oxygen consumption, and mechanical systolic performance may help elucidate the mechanism underlying the observed global LV dysfunction.
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