Myocardial infarction (MI) accounts for most incidences of heart failure (HF) and low ejection fraction. Evidence suggests that acute MI leads to early cardiac remodeling, with changes in ventricular geometry and structure that in turn lead to a vicious cycle of ventricular dilation, increased wall stress, hypertrophy and more ventricular dilation and dysfunction, and worsening of HF. The early geometric and structural changes contribute to early mechanical complications and subsequent progressive ventricular remodeling and the development of chronic HF. A clear understanding of the underlying mechanisms is helpful in developing optimal preventive and therapeutic strategies for HF.
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