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J Thorac Cardiovasc Surg 2008;136:1388-1389
© 2008 The American Association for Thoracic Surgery
Brief Communication |
Division of Cardiac Surgery, Department of Surgery, and Department of Pathology, Toronto General Hospital, University Health Network, University of Toronto, Toronto, Ontario, Canada
Received for publication November 3, 2007; accepted for publication November 30, 2007. * Address for reprints: Ren-Ke Li, MD, PhD, Room 3-702, Toronto Medical Discovery Tower, Toronto General Hospital, 101 College St, Toronto, ON, Canada, M5G 1L7. (Email: renkeli@uhnres.utoronto.ca).
| The first 20% of the full text of this article appears below. |
Cardiac stem cell therapy has received significant attention as a potential biointervention to ameliorate post–myocardial infarction congestive heart failure. Recent prospective randomized clinical trials have provided some evidence showing potential efficacy, although the benefit obtained has been relatively small.1
Thus far, the majority of the evidence suggests that adult stem cells do not cause de novo cardiomyogenesis on a large and reproducible extent. Some have proposed that using embryonic stem cells, which clearly have cardiomyogenic potential, could enhance the beneficial impact of stem cell therapy. Indeed, this may be the case. However, undifferentiated embryonic stem cells are plagued with the potential for teratoma formation.2
To date, this concern has not been an issue for adult-derived stem cells.
We3
recently described the substantial functional benefit of transplanting genetically engineered adult-derived mesenchymal stem cells (MSCs) overproducing stem cell factor (SCF) when transplanted immediately after myocardial infarction. Pressure–volume loop analysis during inferior vena caval occlusion showed a 1.9-fold increase (P < 0.001) in the slope of preload-recruitable stroke work in animals that received MSCs
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