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In some patients acute myocardial infarction and/or infarct expansion induces progressive left ventricular dilatation that eventually leads to heart failure and death. The five year mortality after onset of heart failure is 50%. Chronically stretched viable myocardium adjacent to or remote from an expanding infarction initiates a myopathic process that leads to progressive myocyte apoptosis and adverse postinfarction remodeling. Revascularization of stunned or hibernating myocardium restores contractility and benefits patients in heart failure; however, revascularization does not restore contractility to myopathic, remodeling myocardium. Contemporary operations for heart failure temporarily reduce ventricular wall stress, but fail to reverse stretch induced myocyte apoptosis, which may not be reversible. Logically, prevention of this myopathic process after acute infarction seems required to extend survival. It follows that surgeons should operate before adverse postinfarction left ventricular remodeling occurs, using new operations, rather than afterwards.