Abstract
BackgroundAdverse remodeling of the left ventricle (LV) following myocardial infarction (MI) leads to heart failure. Recent studies have shown that scar anisotropy is a determinant of cardiac function post-MI, however it remains unclear how changes in extracellular matrix (ECM) organization and structure contribute to changes in LV function. The objective of this study is to develop a model to identify potential mechanisms by which collagen structure and organization affect LV function post-MI.MethodsA four-region, multi-scale, cylindrical model of the post-MI LV was developed. The mechanical properties of the infarct region are governed by a constitutive equation based on the uncrimping of collagen fibers. The parameters of this constitutive equation include collagen orientation, angular dispersion, fiber stiffness, crimp angle, and density. Parametric variation of these parameters was used to elucidate the relationship between collagen properties and LV function.ResultsThe mathematical model of the LV revealed several factors that influenced cardiac function post-MI. LV function was maximized when collagen fibers were aligned longitudinally. Increased collagen density was also found to improve stroke volume for longitudinal alignments while increased fiber stiffness decreased stroke volume for circumferential alignments.ConclusionsThe results suggest that cardiac function post-MI is best preserved through increased circumferential compliance. Further, this study identifies several collagen fiber-level mechanisms that could potentially regulate both infarct level and organ level mechanics. Improved understanding of the multi-scale relationships between the ECM and LV function will be beneficial in the design of new diagnostic and therapeutic technologies.
Highlights
Constitutive model The left ventricle (LV) was modeled as a cylindrical membrane formed by folding a planar sheet consisting of three normal, healthy myocardial regions and a collagenous scar region into a cylinder (Figure 1)
In order to investigate the effect of varying the mean fiber angle, an example infarcted LV was run 19 times with the mean fiber angle ranging from 0° to 90°
Simulation results showed that Stroke volume (SV) and ejection fraction (EF) increased with fiber angle and the maximum SV and EF were achieved when the fibers were aligned at 90° (Figure 5A-B)
Summary
Methods Constitutive model The LV was modeled as a cylindrical membrane formed by folding a planar sheet consisting of three normal, healthy myocardial regions and a collagenous scar region into a cylinder (Figure 1). The healthy LV regions were modeled as sheets with nine layers having myocyte fiber angles ranging from −50 to +50 degrees relative to the circumferential direction. W 1⁄4 1 cÀeQ−1Á; ð1Þ with Q 1⁄4 bff Eff þ À bxx Ecc þ Err 2Á þ bfx À E 2 fc þ Ecf. Adverse remodeling of the left ventricle (LV) following myocardial infarction (MI) leads to heart failure. The objective of this study is to develop a model to identify potential mechanisms by which collagen structure and organization affect LV function post-MI. The increased stiffness and diminished contractility of the scar reduce LV function and can lead to heart failure [2]. It is imperative to elucidate the relationship between scar composition and mechanics in order to identify the properties that best preserve LV function
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