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分析特定患者模型中心脏再同步治疗后工作的重新分配。

Analyses of the redistribution of work following cardiac resynchronisation therapy in a patient specific model.

机构信息

Imaging Sciences & Biomedical Engineering Division, King's College London, London, United Kingdom.

出版信息

PLoS One. 2012;7(8):e43504. doi: 10.1371/journal.pone.0043504. Epub 2012 Aug 28.

Abstract

Regulation of regional work is essential for efficient cardiac function. In patients with heart failure and electrical dysfunction such as left branch bundle block regional work is often depressed in the septum. Following cardiac resynchronisation therapy (CRT) this heterogeneous distribution of work can be rebalanced by altering the pattern of electrical activation. To investigate the changes in regional work in these patients and the mechanisms underpinning the improved function following CRT we have developed a personalised computational model. Simulations of electromechanical cardiac function in the model estimate the regional stress, strain and work pre- and post-CRT. These simulations predict that the increase in observed work performed by the septum following CRT is not due to an increase in the volume of myocardial tissue recruited during contraction but rather that the volume of recruited myocardium remains the same and the average peak work rate per unit volume increases. These increases in the peak average rate of work is is attributed to slower and more effective contraction in the septum, as opposed to a change in active tension. Model results predict that this improved septal work rate following CRT is a result of resistance to septal contraction provided by the LV free wall. This resistance results in septal shortening over a longer period which, in turn, allows the septum to contract while generating higher levels of active tension to produce a higher work rate.

摘要

调节区域性工作对于高效的心功能至关重要。在心力衰竭和电功能障碍(如左束支传导阻滞)的患者中,室间隔的区域性工作通常会降低。心脏再同步治疗(CRT)后,通过改变电激活模式,可以重新平衡这种不均匀的工作分布。为了研究这些患者的区域性工作变化以及 CRT 后功能改善的机制,我们开发了一个个性化的计算模型。模型中的机电心脏功能模拟估计 CRT 前后的区域性应力、应变和做功。这些模拟预测,CRT 后观察到的室间隔做功增加不是由于收缩过程中募集的心肌组织体积增加所致,而是募集的心肌体积保持不变,单位体积的平均峰值做功率增加。这种峰值平均做功率的增加归因于室间隔收缩的速度变慢且更有效,而不是主动张力的变化。模型结果预测,LV 游离壁提供的阻力导致 CRT 后改善的室间隔工作率。这种阻力导致室间隔在更长的时间内缩短,从而使室间隔在产生更高水平的主动张力以产生更高的做功率的同时进行收缩。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/ef95/3429501/31dffcba3a2f/pone.0043504.g001.jpg

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