LETTERS TO THE EDITOR
Reply
Jutta Schaper, MD, PhD* and
Albrecht Elsasser, MD
* Max-Planck-Institut, Exp. Cardiology, Benekestr.2, D-61231 Bad Nauheim, Germany (Email: j.schaper{at}kerckhoff.mpg.de).
We thank Dr. Abbate and colleagues for their interest in our work (1). The major point of our recent publication is the fact that autophagic cell death as described previously in patients with dilated cardiomyopathy (2) is an important mechanism for killing myocytes in hibernating myocardium and that apoptosis seems to be of less importance. We are fully aware of the many technical problems that might occur when attempting a quantitative analysis of the rate of cell death, be it apoptosis, autophagic cell death, or necrosis (3). In our experience, electron microscopy is not a suitable method for determining the rate of cell death, which has been emphasized by others as well (4). Therefore, we use the confocal microscope. We analyze entire sections, and as many cells as are available from the patient's material; we count the total number of nucleated myocytes per patient and we determine the number of specifically labeled cells. This information is then statistically analyzed on the basis of individual data from each patient and ultimately expressed as a percentage. In a final stage, results are summarized for an entire group of patients, and different groups are compared by employing appropriate statistical tests. Using this procedure each patient is weighted equally, even if there are no labeled cells present.
We read with interest Dr. Abbate and colleagues' work on myocardial apoptosis in patients with unfavorable left ventricular remodeling and we noticed the unusually high rates of apoptosis reported for both infarcted myocardium and areas remote from the infarct (5). Unfortunately, a precise indication of the total number of myocytes examined is lacking from the description of methods, rendering difficult an interpretation of these results. It would have been more convincing had Dr. Abbate and colleagues used the same criteria in his own work that he requests from ours.
There is no doubt, however, that myocyte death is a major contributing factor to the deterioration of cardiac function in pathological situations in the human heart, either in postinfarction remodeling or in hibernating myocardium.
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References
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1. Elsasser A, Vogt AM, Nef HM, et al. Human hibernating myocardium is jeopardized by apoptotic and autophagic cell death J Am Coll Cardiol 2004;43:2191-2199.[Abstract/Free Full Text]
2. Kostin S, Pool L, Elsasser A, et al. Myocytes die by multiple mechanisms in failing human hearts Circ Res 2003;92:715-724.[Abstract/Free Full Text]
3. Elsasser A, Suzuki K, Schaper J. Unresolved issues regarding the role of apoptosis in the pathogenesis of ischemic injury and heart failure J Mol Cell Cardiol 2000;32:711-724.[CrossRef][Web of Science][Medline]
4. Anversa P. Myocyte death in the pathological heart Circ Res 2000;86:121-124.[Free Full Text]
5. Abbate A, Biondi-Zoccai GG, Bussani R, et al. Increased myocardial apoptosis in patients with unfavorable left ventricular remodeling and early symptomatic postinfarction heart failure J Am Coll Cardiol 2003;41:753-760.[Abstract/Free Full Text]
Related Article
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Hibernating myocardium, apoptosis, and a simple mathematical task
- Antonio Abbate, Giuseppe Biondi-Zoccai, Pierfrancesco Agostoni, Luigi M. Biasucci, Alfonso Baldi, and Filippo Crea
J. Am. Coll. Cardiol. 2005 45: 466.
[Full Text]
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