Decompensated eccentric ventricular hypertrophy characterizes the tran
sition from compensated pressure or volume overload hypertrophy to myo
cardial dysfunction and failure. Myocyte loss is the major etiologic f
actor of wall thinning and chamber dilation and may condition the prog
ression of the cardiac myopathy. Myocyte death can occur by apoptosis
or necrosis, but the activation of the suicide program of myocytes exc
eeds necrotic cell death in the pathologic heart of ischemic origin. W
hether reactive fibrosis constitutes a primary event in the initiation
of ventricular dysfunction or a secondary reaction to myocyte death i
s an important unanswered question.