Toward antiapoptosis as a new treatment modality.

Despite successful new treatment strategies developed in the past few decades aimed at different pathomechanisms of myocardial disease,1 morbidity and mortality due to heart failure and its complications remain a clinical reality. Among the treatment strategies available, the maintenance of contractile mass that is determined by the number of myocytes and the degree of cellular hypertrophy is a major goal in the therapy of cardiac disease. However, increasing contractile mass by myocardial hypertrophy is associated with increased risks of vulnerability to ischemia, arrhythmias, and the transition to heart failure. Recent evidence that apoptosis of cardiac myocytes is a feature in several myocardial disease states, including ischemic heart disease and congestive heart failure (for review, see Reference 2), has raised hopes that inhibition of myocyte apoptosis could prevent or slow the loss of contractile cells and thus provide a new target in a multimodal therapeutic approach to cardiac disease.