Dilated cardiomyopathy (DCM) has emerged as a major health problem dur
ing the past two decades In spite of recent advances, it has become cl
ear that the underlying heart disease is relentlessly progressive in a
lmost all patients who develop symptoms of overt failure; morbidity an
d mortality continues to be unacceptably high with an incidence of app
roximately approximately 30% for death or hospital admission at one ye
ar. Cardiac transplantation remains the only current prospect for dram
atically improving survival in many patients. Trying to enhance cardia
c function during the later stages of heart failure is ultimately frui
tless; it cannot be done over the long term. The solution to failure l
ies in defining and preventing its causes or arresting and reversing i
ts evolution. We propose a model where the target for therapeutic inte
rvention becomes the arrest of progressive myocardial disease througho
ut the course of the the cardiomyopathy. In this paradigm, the selecti
on of therapeutic agents for the treatment of heart failure takes into
consideration both the stage of the disease and differences in pathog
enesis. In addition it broadens our approach from one which focuses on
enhancing myocardial function to one which encompasses strategies whi
ch are designed to inhibit the progressive loss of myocytes and the in
exorable deterioration of the failing myocardium.