Heart disease is a leading cause of death worldwide, and coronary heart disease causes 1 of every 6 deaths in the United States [1]. Following a myocardial infarction, scar tissue gradually replaces myocardium that is lost through a process of collagen deposition and an increase in tensile strength of the tissue [2]. This leads to infarct expansion, adverse ventricular remodeling and dysfunction, and ultimately heart failure. Dilation of the left ventricle (LV) leads to increased LV wall stress and is ultimately responsible for adverse ventricular remodeling. LV dilation causes stretching and thereby increased wall stress, prohibiting cardiomyocytes from effectively contracting, which leads to further dilation, and ultimately a decrease in cardiac pump efficiency [3]. Previously, it has been shown that using a tissue filler to modify the material properties of an infarct limits the process of ventricular remodeling [4]. Angiogenesis is another mechanism by which adverse ventricular remodeling can be limited. Previously, our group developed engineered stromal cell-derived factor-1α (ESA), a computationally designed analog of an established endothelial progenitor cell chemokine, SDF-1α, and demonstrated that ESA injection enhances LV function by promoting angiogenesis and retains the native properties of the extracellular matrix (ECM) [5] [6]. In this study, we propose that injection of ESA to infarcted cardiac muscle improves the tensile strength and viscoelastic properties of ventricular muscle.

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