{"title":"Letter to the editor--multifocal myocardial apoptoses: distinctive cardiac lesions in cystic fibrosis and other diseases.","authors":"Jiri T Beranek","doi":"10.1080/pdp.22.2.187.188","DOIUrl":null,"url":null,"abstract":"Being interested in the mechanism of cardiomyocyte cell death [1], I have read with attention the article by Nezelof et al. [in this publication; 2] about multifocal myocardial necrosis in cystic ¢brosis and other diseases.Today, it is known that necrosis, called more suitably accidental cell death, leads to in£ammatory reaction whereas apoptosis, the secondmechanismof cell death, does notprovoke in£ammation. Since there is no in£ammatory reaction in the cases described by Nezelof et al. [2], wemayask justi¢ably whether the cardiomyocytes in question have not died by apoptosis instead of necrosis. Indeed, cardiomyocyte apoptosis is present in F|gure 2 of the article [2].Numerous atrophic cardiomyocytes are scattered amid di¡use ¢brosis in the upper two thirds of the ¢gure. Amajority of themmanifest a fragmentation into small apoptotic bodies. The reader may be mislead by their similarity to vessels ¢lled with red cells [1], a phenomenon already described in the hearts of systemic sclerosis patients [3]. Acarefulmorphologic analysis shows, however, that apoptoticbodies are inside cardiomyocytes and cannot be, therefore, red cells. In the bottom third of F|gure 2, cardiomyocytes are less damaged and it is easy to ¢nda clearly recognizable myo¢ber fragmenting into apoptoticbodies [2].The lackof in£ammatory reaction in F|gure 2 also con¢rms the conclusion that the cardiomyocytes in question are dying by apoptosis [2]. F|gures1, 3, and 4 are, unfortunately, of too lowmagni¢cation tovisualize cellular details [2].They show, however, numerousmyocardial clefts that are not present in the normal heart and that often contain tissue remains.The latter may be either artefacts (the shrunken interstitium) or deadcardiomyocytes. I would advance that the second alternative is true because the tissue remains often manifest similar tinctorial properties as surrounding them, cardiomyocytes and=or contain dark small apoptototic bodies inside them. Again, the lack of in£ammatory reaction indicates","PeriodicalId":82276,"journal":{"name":"Pediatric pathology & molecular medicine","volume":"22 2","pages":"187-8"},"PeriodicalIF":0.0000,"publicationDate":"2003-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1080/pdp.22.2.187.188","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pediatric pathology & molecular medicine","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1080/pdp.22.2.187.188","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Being interested in the mechanism of cardiomyocyte cell death [1], I have read with attention the article by Nezelof et al. [in this publication; 2] about multifocal myocardial necrosis in cystic ¢brosis and other diseases.Today, it is known that necrosis, called more suitably accidental cell death, leads to in£ammatory reaction whereas apoptosis, the secondmechanismof cell death, does notprovoke in£ammation. Since there is no in£ammatory reaction in the cases described by Nezelof et al. [2], wemayask justi¢ably whether the cardiomyocytes in question have not died by apoptosis instead of necrosis. Indeed, cardiomyocyte apoptosis is present in F|gure 2 of the article [2].Numerous atrophic cardiomyocytes are scattered amid di¡use ¢brosis in the upper two thirds of the ¢gure. Amajority of themmanifest a fragmentation into small apoptotic bodies. The reader may be mislead by their similarity to vessels ¢lled with red cells [1], a phenomenon already described in the hearts of systemic sclerosis patients [3]. Acarefulmorphologic analysis shows, however, that apoptoticbodies are inside cardiomyocytes and cannot be, therefore, red cells. In the bottom third of F|gure 2, cardiomyocytes are less damaged and it is easy to ¢nda clearly recognizable myo¢ber fragmenting into apoptoticbodies [2].The lackof in£ammatory reaction in F|gure 2 also con¢rms the conclusion that the cardiomyocytes in question are dying by apoptosis [2]. F|gures1, 3, and 4 are, unfortunately, of too lowmagni¢cation tovisualize cellular details [2].They show, however, numerousmyocardial clefts that are not present in the normal heart and that often contain tissue remains.The latter may be either artefacts (the shrunken interstitium) or deadcardiomyocytes. I would advance that the second alternative is true because the tissue remains often manifest similar tinctorial properties as surrounding them, cardiomyocytes and=or contain dark small apoptototic bodies inside them. Again, the lack of in£ammatory reaction indicates