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This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Christof Stamm Roland Hetzer Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Stamm, C. Articles by Hetzer, R. Search for Related Content PubMed Articles by Stamm, C. Articles by Hetzer, R. Related Collections Myocardial infarction Related Article

J Thorac Cardiovasc Surg 2007;134:1095-1096
© 2007 The American Association for Thoracic Surgery

Letter to the Editor

Rescue versus regeneration

Deutsches Herzzentrum Berlin, Cardiothoracic and Vascular Surgery, Berlin, Germany

To the Editor:

We read with interest the article by Suzuki and colleagues,¹ in which they examined the effects of mechanical unloading on self-regeneration of the injured heart. The model they used is a very good example of how classic surgical techniques can help answer current basic research questions. There is no doubt as to the validity of the main finding, namely, that taking the hemodynamic load off an acutely ischemic and failing heart is beneficial. We² have followed this strategy in the clinical setting for some time now. The one problem that we see in the authors’ conclusion is perhaps merely semantic, but still deserves consideration. Throughout the article, regeneration processes are discussed that are believed to involve intrinsic stem cells, stem cell migration from the periphery or mitotic cardiomyocyte replication. However, we believe that it is very important to distinguish between the biology of myocardial rescue and that of "true" regeneration. This may be difficult based on the data from Suzuki and colleagues’ article, because they unloaded the hearts as early as 1 hour after the onset of infarction. Among many other things, removing the work load markedly reduces oxygen consumption of the myocardium (reflected, for instance, by a downregulation of respiratory chain enzymes),³ with obvious beneficial effects on cell survival. These effects are probably most pronounced in the mechanically and biologically overburdened infarct border zone. Therefore, it does not seem surprising that the authors found less apoptosis and more markers of vital cells—including c-kit– and Sca-1–expressing cells—right there. To study true regeneration processes, however, unloading of the hearts later after myocardial infarction might produce more meaningful data. Here, the effects of myocardial rescue by unloading have abated, enabling the researcher to concentrate on true regeneration processes instead of salvage of pre-existing cells. We expect that the differences in regenerative capacity between unloaded and loaded hearts would then be much smaller, similar to the clinical observation that weaning from left ventricular assist device support during acute infarction or in nonischemic cardiomyopathy is sometimes possible,⁴ but very rarely in patients with chronic ischemic heart failure.

Taken together, the data presented by Suzuki and colleagues add nicely to the evidence supporting the concept of rapid hemodynamic load reduction in acute infarction. Whether unloading alone is able to also initiate true myocardial regeneration, especially in the clinical setting, remains to be seen.

References

1. Suzuki R, Li TS, Mikamo A, Takahashi M, Ohshima M, Kubo M, et al. The reduction of hemodynamic loading assists self-regeneration of the injured heart by increasing cell proliferation, inhibiting cell apoptosis, and inducing stem-cell recruitment. J Thorac Cardiovasc Surg 2007;133:1051-1058.[Abstract/Free Full Text]
   
2. Potapov EV, Weng Y, Hausmann H, Kopitz M, Pasic M, Hetzer R. New approach in treatment of acute cardiogenic shock requiring mechanical circulatory support. Ann Thorac Surg 2003;76:2112-2114.[Abstract/Free Full Text]
   
3. Bugger H, Leippert S, Blum D, Kahle P, Barleon B, Marme D, et al. Subtractive hybridization for differential gene expression in mechanically unloaded rat heart. Am J Physiol Heart Circ Physiol 2006;291:H2714-H2722.[Abstract/Free Full Text]
   
4. Dandel M, Weng Y, Siniawski H, Potapov E, Lehmkuhl HB, Hetzer R. Long-term results in patients with idiopathic dilated cardiomyopathy after weaning from left ventricular assist devices. Circulation 2005;112(9 Suppl):I37-I45.[Medline]
   

This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Christof Stamm Roland Hetzer Permission Requests Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Stamm, C. Articles by Hetzer, R. Search for Related Content PubMed Articles by Stamm, C. Articles by Hetzer, R. Related Collections Myocardial infarction Related Article