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Monitoring Stem Cell Research 
cardiomyocytes against apoptosis, induction of cardiomyocyte 
proliferation and regeneration, long-term salvage and survival of 
viable myocardium, prevention of left ventricular remodelling and 
sustained improvement in cardiac function. It is reasonable to 
anticipate that cell therapy strategies for ischemic heart disease will 
need to incorporate (1) a renewable source of proliferating, functional 
cardiomyocytes, and (2) angioblasts to generate a network of 
capillaries and larger size blood vessels for supply of oxygen and 
nutrients to both the chronically ischemic endogenous myocardium 
and to the newly-implanted cardiomyocytes. 
Introduction 
Congestive heart failure remains a major public health 
problem, with recent estimates indicating that end-stage heart 
failure with two-year mortality rates of 70-80% affects over 60,000 
patients in the US each year \ In Western societies heart failure is 
primarily the consequence of previous myocardial infarction As 
new modalities have emerged which have enabled significant 
reduction in early mortality from acute myocardial infarction, 
affecting over 1 million new patients in the US annually, there has 
been a paradoxical increase in the incidence of post-infarction heart 
failure among the survivors. Current therapy of heart failure is 
limited to the treatment of already established disease and is 
predominantly pharmacologiced in nature, aiming primarily to inhibit 
the neurohormonal axis that results in excessive cardiac activation 
through angiotensin- or norepinephrine-dependent pathways. For 
patients with end-stage heart failure treatment options are extremely 
limited, with less than 3000 being offered cardiac transplants 
annually due to the severely limited supply of donor organs and 
implantable left ventricular assist devices (LVADs) being expensive, 
not proven for long-term use, and associated with significant 
complications Clearly, development of approaches that prevent 
heart failure after myocardial infarction would be preferable to those 
that simply ameliorate or treat already established disease. 
Heart Failure After Myocardial Infarction Results From 
Progressive Ventricular Remodelling. Heart failure after myocardial 
infarction occurs as a result of a process termed myocardial 
remodelling. This process is characterized by myocyte apoptosis, 
cardiomyocyte replacement by fibrous tissue deposition in the 
ventricular wall progressive expansion of the initial infarct area 
and dilation of the left ventricular lumen Another integral 
component of the remodelling process appears to be the 
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