Congestive heart failure (CHF) evolves either from an excessive workload or in response to loss of myocardium, both of which cause cardiac hypertrophy, increased cardiac pressure, and loss of functional reserve. Nearly 60% of patients in heart failure present with ischemic cardiomyopathy, which in its chronic form exhibits biventricular dilatation, elevated left ventricular mass, and extensive large-vessel atherosclerosis. The hypertrophy is proportional to the loss of myocardium, although animal studies suggest this varies with the infarct size. However, recent studies indicate that early afterload reduction may relieve the hypertrophic stimulus and prevent degeneration. Some 30% to 40% of patients in heart failure present with an idiopathic dilated cardiomyopathy, with a patchy but diffuse loss of tissue on microscopy, reactive hypertrophy in the surviving cells, and interstitial fibrosis and replacement scarring. The ultrastructural changes still await clarification. The role of pharmacologic intervention still remains unclear. However, any reduction in mortality will necessitate the identification of those cellular changes that inevitably lead to secondary degeneration of the remaining viable myocardium.