ABSTRACT
The incidence of congestive heart failure (HF) is increasing with epidemic proportions,
occurring most frequently in patients with structural heart disease resulting from
myocardial infarction (MI). The process of cardiac remodeling, which provides a substrate
for HF, results from fibrotic scar formation that replaces regions of myocyte necrosis
coupled with insufficient endogenous repair responses. In addition, surviving myocytes
undergo hypertrophy, which may be initially beneficial but transitions to a maladaptive
process in which myocytes become vulnerable to apoptosis. The heart dilates due to
infarct expansion, with wall thinning and dilatation, hyperplasia of fibroblasts, and scar
formation, changes its geometry and loses contractile function-the defining features of
ventricular remodeling (1). While cardiomyocytes may not be terminally differentiated
and endogenous cardiac stem cells are now identified within the heart (2-5), it is clear
from these clinical sequellae that endogenous repair mechanisms are insufficient to
adequately allow the heart to heal structurally and functionally from MI.
