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Editorials |
From the Department of Cell Biologyl Department of Cardiovascular Medicine; Department of Biomedical Engineering; Cleveland Clinic Foundation, Cleveland, Ohio.
Correspondence to Marc S. Penn, MD, PhD, Director, Bakken Heart-Brain Institute, Departments of Cardiovascular Medicine and Cell Biology, NE3, 9500 Euclid Avenue, Cleveland, OH 44195. E-mail pennm@ccf.org
See related article, pages 12341241
Key Words: chronic heart failure stem cells biomarkers
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
Recent clinical trials have demonstrated the safety and potential benefits of the stem cell based therapies for the preservation and treatment of cardiac dysfunction following acute myocardial infarction.1,2 More recently Assmus and colleagues published the TOPCARE-CHD trial in which they compared the effects of infusing circulating progenitor cells to bone marrow mononuclear cells in patients at a time remote from acute myocardial infarction (average time from AMI to infusion, 6 to7 years).3 Using a crossover clinical trial design that study demonstrated that circulating progenitor cells offered no benefit, where as infusion of whole bone marrow mononuclear cells resulted in an increase of 2.9% in the ejection fraction compared with a loss of 1.2% in control patients.3 The observation that circulating progenitor cells and bone marrow mononuclear cells lead to improved function in acute myocardial infarction,4 but only bone marrow derived progenitor cells led to improvement at times significantly remote from AMI suggest that different cell populations or delivery strategies may be efficacious in one setting but not another. For example, CD34+ cells are present in both circulating progenitor cells and whole bone marrow mononuclear preparations, mesenchymal stem cells are only present in the bone derived progenitor cell preparations.
Similarly, the literature to date has demonstrated critical differences between myocardial tissue immediately after and that at times remote from an acute ischemic event with respect to the expression of stem cell homing factors, inflammatory infiltrates and putative differentiation factors.5,6,7 Thus, although CD34+ cells may be able to home to myocardial tissue
Related Article:
Circ. Res. 2007 100: 1234-1241.
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