The American Heart Association reported that in 2004 alone, myocardial infarction (MI) related mortality rate was as high as 38% among the 1.2 million reported MI cases [1]. After an MI, the self-repair capability of the infarcted heart is limited. As a result, the heart undergoes a remodeling process, characterized by progressive weakening of contractile function. It is believed that increased left ventricular (LV) loading to survival myocytes post-MI activates the apoptotic pathways in the cells, leading to progressive loss of cardiomyocytes.

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