The Role of Infarct Stiffness in Cardiac Patch Therapy: A Computational Study Using an Idealized Left Ventricular Geometry.

Tissue-engineered contractile patches offer a promising therapeutic strategy to restore cardiac function following myocardial infarction (MI) and mitigate adverse ventricular remodeling, a key contributor to the progression of heart failure (HF). However, experimental and numerical studies indicate that their functionality may be affected by the mechanical properties of the underlying infarct. In this computational study, we investigate how infarct tissue stiffness and wall thickness influence the ability of a contractile cardiac patch to restore cardiac function. A model of cardiac mechanics was used to model MI in a region comprising 15% of the left ventricle. In this region, active stress generation was eliminated, and passive tissue stiffness and wall thickness were varied. The cardiac patch was modeled as a rectangular piece of healthy myocardium with a volume of 25% of the infarcted tissue. Following MI, stroke work decreased by 32% compared to the healthy heart. This loss increased with increasing infarct tissue stiffness and decreasing infarct wall thickness. In the most favorable case, the cardiac patch restored up to 15% of this loss, of which about one-third was attributed to a direct contribution of the patch and two-thirds to improved function in adjacent healthy myocardium. Decreasing tissue stiffness improved restoration of cardiac pump function and the relative contribution of the patch. Conversely, while reduced wall thickness improved restoration of pump function, it decreased the relative contribution of the patch. Lower infarct stiffness, either through tissue stiffness or wall thinning, allows more cardiac function to be restored via patch implantation.