Mobilization of bone marrow-derived stem cells after myocardial infarction and left ventricular function: simply effects of optimized drug treatment?

Thomas Thum

Bayrische Julius-Maximilians-Universität
Medizinische Klinik
Josef-Schneider Str. 2
97080 Würzburg
Germany
Tel: +49 931 201 36154
Fax: +49 931 201 36953
E-mail address:
Thum_T{at}klinik.uni-wuerzburg.de

Johann Bauersachs

Bayrische Julius-Maximilians-Universität
Medizinische Klinik
Josef-Schneider Str. 2
97080 Würzburg
Germany

We read with interest the recent article by Leone et al.1 regarding the mobilization of CD34+ cells from bone marrow after myocardial infarction (MI) and the effects on left ventricular function.

ACE-inhibitors and statins are administered on a routine basis to patients with acute MI and are likely to contribute to enhance levels of CD34+ cells.2,3 Indeed, the present paper identifies the use of statins after MI as the best independent predictor of increased mobilization of stem cells. In animal models, however, Nygren et al.4 were unable to detect any increase in peripheral blood progenitor or stem cell activity following MI when animals were without drug treatment. These findings could not be attributed to the trapping of potentially mobilized cells, as no progenitor cells were detected in the infarcted myocardium or in the spleen. Likewise, the findings of Leone et al.1 that 1 year after MI the levels of CD34+ cells were still three-fold higher when compared with the time before MI are difficult to explain by MI or acute release of inflammatory mediators which mobilize stem cells such as VEGF. We postulate that these findings are the result of an optimized drug therapy of patients following MI, including the use of statins, ACE-inhibitors, and other potentially stem cell-mobilizing agents. The finding of Leone et al.1 that the amount of mobilized stem cells is highly variable and does not correlate to the size and severity of MI also points to a multimodal regulation of stem cell mobilization after MI. Interestingly, the finding that CD34+ cell concentration was an independent predictor for global and regional improvement of the left ventricular function 1 year after MI, but not early after MI, may suggest that CD34+ cells could be used as a diagnostic tool to identify patients with a high risk of developing heart failure after MI and who should therefore receive specifically intensive drug therapy.

References

  1. Leone AM, Rutella S, Bonanno G, Abbate A, Rebuzzi AG, Giovanni S, Lombardi M, Galiuto L, Liuzzo G, Andreotti F, Lanza GA, Contemi AM, Leone G, Crea F. Mobilisation of bone marrow derived stem cells after myocardial infarction and left ventricular function. Eur Heart J 2005;26:1196–1204.[Abstract/Free Full Text]
  2. Dimmeler S, Aicher A, Vasa M, Mildner-Rihm C, Adler K, Tiemann M, Rutten H, Fichtlscherer S, Martin H, Zeiher AM. HMG-CoA reductase inhibitors (statins) increase endothelial progenitor cells via the PI 3-kinase/Akt pathway. J Clin Invest 2001;108:391–397.[Abstract/Free Full Text]
  3. Min TQ, Zhu CJ, Xiang WX, Hui ZJ, Peng SY. Improvement in endothelial progenitor cells from peripheral blood by ramipril therapy in patients with stable coronary artery disease. Cardiovasc Drugs Ther 2004;18:203–209.[CrossRef][ISI][Medline]
  4. Nygren JM, Jovinge S, Breitbach M, Sawen P, Roll W, Hescheler J, Taneera J, Fleischmann BK, Jacobsen SE. Bone marrow-derived hematopoietic cells generate cardiomyocytes at a low frequency through cell fusion, but not transdifferentiation. Nat Med 2004;10:494–501.[CrossRef][ISI][Medline]




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