See related article, pages 159–167 Heart failure is a major worldwide health problem that is growing in prevalence despite recent treatment advances. Patients with heart failure ultimately die from either pump failure or cardiac arrhythmia, and there is a link between the degree of contractile dysfunction and arrhythmic risk. Since the 1960s, the definitive therapy for heart failure has been cardiac transplantation, but the limited supply of organs has restricted the impact of this therapy. Starting in the mid-1990s, a series of observations has led to the concept that cells might be used to repair myocardial damage. Subsequently, this therapy has shown promise in ischemic and nonischemic forms of myocardial injury. The increased availability of cells as compared with organs has driven an exuberant search for the right replacement cells. Nevertheless, after intense study, there is no obvious frontrunner.1 The concept driving the cell selection process has been the need for a sufficient number of immune compatible, contractile cells. Proposed cell sources have included skeletal myoblasts,2 bone marrow–derived progenitor cells,3 and embryonic stem cells.4 These 3 cell types have been shown to improve myocardial function in animal models, and the first 2 have shown promise in human clinical trials.5 Generally, the effects of these 2 cell types on myocardial function have been similar.6 If they are to fulfill their promise as replacement myocytes, it is important that the …
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