A single strain-based growth law predicts concentric and eccentric cardiac growth during pressure and volume overload.
A single strain-based growth law predicts concentric and eccentric cardiac growth during pressure and volume overload.
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DOI：
10.1016/j.mechrescom.2011.11.004
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发表时间：
2012-06-01
影响因子：
2.4
通讯作者：
McCulloch AD
中科院分区：
文献类型：
--
作者：
Kerckhoffs RC;Omens J;McCulloch AD
成人心肌通过生长和重塑(G&R)通过多种机制适应环境中的机械性变化。当心脏承受慢性机械超负荷时，就会发生肥厚。在室压超负荷时(例如，由于主动脉狭窄)，心脏典型的反应是同心性肥大，特征是当肌节平行加入时，由于肌细胞放射状生长导致室壁增厚。在心室容量超负荷时，充盈压力的增加(例如由于二尖瓣返流)会导致偏心性肥厚，因为心肌细胞通过连续增加肌节而轴向生长，从而导致室腔扩大，通常伴随着一些室壁增厚。刺激不同模式的心室肥厚的特定生物力学刺激仍然知之甚少。在最近的一项研究中，基于微图案化的心肌细胞培养受到拉伸的体外研究，我们提出，心肌细胞生长更长，以保持较好的肌节长度，以响应增加的纤维应变；生长更厚，以保持丝间点阵间距，以响应增加的跨纤维应变。在这里，我们在成年犬心脏的计算模型和循环血流动力学的闭环模型中，测试这种生长规律是否能够分别预测向心性肥厚和偏心性肥厚对主动脉瓣狭窄和二尖瓣反流的响应。建立了犬脑室搏动与循环耦合的非线性有限元模型。在引起瓣膜改变后，随着时间的推移，脑室被允许适应机械刺激的形状。当与压力超负荷和容量超负荷的犬心脏的综合模型结合在一起时，所提出的生长规律能够再现主要的急性和慢性生理反应(结构和功能)，再加上闭合循环。我们得出结论，基于应变的生物力学刺激可以推动心脏生长，包括压力超负荷期间的室壁增厚。
Adult cardiac muscle adapts to mechanical changes in the environment by growth and remodeling (G&R) via a variety of mechanisms. Hypertrophy develops when the heart is subjected to chronic mechanical overload. In ventricular pressure overload (e.g. due to aortic stenosis) the heart typically reacts by concentric hypertrophic growth, characterized by wall thickening due to myocyte radial growth when sarcomeres are added in parallel. In ventricular volume overload, an increase in filling pressure (e.g. due to mitral regurgitation) leads to eccentric hypertrophy as myocytes grow axially by adding sarcomeres in series leading to ventricular cavity enlargement that is typically accompanied by some wall thickening. The specific biomechanical stimuli that stimulate different modes of ventricular hypertrophy are still poorly understood. In a recent study, based on in-vitro studies in micropatterned myocyte cell cultures subjected to stretch, we proposed that cardiac myocytes grow longer to maintain a preferred sarcomere length in response to increased fiber strain and grow thicker to maintain interfilament lattice spacing in response to increased cross-fiber strain. Here, we test whether this growth law is able to predict concentric and eccentric hypertrophy in response to aortic stenosis and mitral valve regurgitation, respectively, in a computational model of the adult canine heart coupled to a closed loop model of circulatory hemodynamics. A non-linear finite element model of the beating canine ventricles coupled to the circulation was used. After inducing valve alterations, the ventricles were allowed to adapt in shape in response to mechanical stimuli over time. The proposed growth law was able to reproduce major acute and chronic physiological responses (structural and functional) when integrated with comprehensive models of the pressure-overloaded and volume-overloaded canine heart, coupled to a closed-loop circulation. We conclude that strain-based biomechanical stimuli can drive cardiac growth, including wall thickening during pressure overload.
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影响因子：
3.3
作者：
Holmes, JW
通讯作者：
Holmes, JW
影响因子：
3.8
作者：
Gopalan, SM;Flaim, C;McCulloch, AD
通讯作者：
McCulloch, AD
影响因子：
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作者：
Eyster, JAE;Meek, WJ;Hodges, FJ
通讯作者：
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影响因子：
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作者：
ENRIQUEZSARANO, M;SCHAFF, HV;FRYE, RL
通讯作者：
FRYE, RL
DOI：
10.1152/ajpheart.1995.269.6.h2065
发表时间：
1995-12-01
影响因子：
4.8
作者：
DellItalia, LJ;Meng, QC;Elton, TS
通讯作者：
Elton, TS