Several investigators have been successful in reducing the adverse left ventricular (LV) remodeling and expansion that exists in response to myocardial infarction (MI) via the use of various restraints, such as knitted polypropylene meshes [1] and injectable materials [2]. A recent finite element model simulation of the theoretical impact of injection of a material into the myocardium after MI confirmed the suspected stress reduction potential of intramyocardial infarct stiffening with an acellular, non-contractile material. As peak LV wall stress has been implicated in the pathogenesis of post-infarct LV remodeling, this approach to LV wall stress reduction has significant therapeutic potential [3].

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