Over one million patients are affected with left ventricular (LV) injury annually after sustaining a myocardial infarction (MI). In order to compensate for the loss in pumping function, the heart undergoes changes meant to maintain homeostasis. This process actually leads to a remodeling process that is initially compensatory and later becomes maladaptive. Remodeling after MI often involves loss of contractility and hypertrophy of the LV in response to increased loading conditions. Some patients are able to recover with the use of medicine and surgical intervention. However, others experience a progression of the remodeling process which leads to LV dysfunction and heart failure as the heart becomes more spherical and loses its ability to effectively contract. [1]

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