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Correspondence |
Columbia, Missouri
To the Editor-in-Chief:
A delayed reaction to published research occurs when new advances permit a novel look at previously accepted concepts.1,2 This explains my interest in the article by Erlich et al3 about the influence of tissue factor-thrombin pathway on myocardial ischemia-reperfusion injury. Using rabbits, the authors created ischemia in the region supplied by the anterolateral branch of the left main coronary for 45 minutes and reperfused the ischemic region for 2 hours. At the end of the experiments, the animals were sacrificed and studied morphologically.
In Figure 5A of the article by Erlich et al,3 an area of ischemic and reperfused myocardium is identified by acid-fuchsin staining. It contains numerous myocardial defects, indicating that the myocardium has not only been heavily damaged but that numerous cardiomyocytes have also disappeared. What was the mechanism of their destruction? Accidental death, sometimes called necrosis, may be excluded because of the shortness of time. Only apoptosis comes into consideration. Sessile macrophages are able to phagocytize apoptotic bodies of a cardiomyocyte in a few hours. It is doubtful, however, that they would be able to create myocardial defects so numerous and large in such a short time as in Figure 5A without the help of their counterparts from blood and the bone marrow. Being a part of chronic inflammatory reaction, the intervention of blood and bone marrow macrophages may also be excluded by reason of the shortness of time. There is only one possibility left which is cardiomyocyte apoptosis and the elimination of apoptotic bodies by lymphatic outflow.4
In Figure 5A, myocardial defects contain small particles which may be red cells or cardiomyocyte apoptotic bodies.5 The answer to this question may be found in Figure 5, B and C, which also visualize ischemic and reperfused areas. There, it is distinctly visible that: tissue factor is located not only in the sarcolemma and intercalated disks but also in cardiomyocyte cytoplasm; the same particles as those in myocardial defects are also present inside clearly recognizable fragmenting cardiomyocytes; and any of these particles contain tissue factor. Consequently, a majority of them are not red cells but cardiomyocyte apoptotic bodies.
Small eosinophilic particles present in histological slides of cardiac hyperacute rejection1 and reperfusion injury5 have usually been considered to be red cells forming interstitial hemorrhage. We have observed, however, that their appearance is almost always accompanied by a disappearance of cardiomyocytes. Having observed their formation inside fragmenting cardiomyocytes, we concluded that they derived from them eosinophilic droplets.6 Only later, we hypothesized that they were cardiomyocyte apoptotic bodies5 and that they played an important role in fundamental processes of cardiac pathology such as reperfusion injury5 and postinfarction heart rupture.7 This letter brings evidence that tissue factor may help us to distinguish between cardiomyocyte apoptotic bodies and interstitial hemorrhage.
References
This article has been cited by other articles:
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  J. T. Beranek, T. El-Sawy, and R. L. Fairchild Unusual Apoptosis in Experimental Cardiac Rejection Am. J. Pathol., December 1, 2003; 163(6): 2640 - 2642. [Full Text]
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