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Ann Thorac Surg 2005;79:1095
© 2005 The Society of Thoracic Surgeons

Correspondence

MCC-135 Diminishes the Egress of CK-MB but Not of Troponin-I From Cardiomyocytes During Reperfusion

Jiri T. Beranek, MD

4101 S Wappel Dr, Columbia, MO 65203, USA

jiriberanek{at}hotmail.com

To the Editor:

Apoptosis eliminates injured cells without inflammation. It is in the interest of the organism that injured cardiomyocytes die by apoptosis and not oncosis or that they do not die at all. High intracellular levels of Ca2+ promote oncosis, and lower levels promote apoptosis [1]. Yarbrough and associates [2] used a calcium modulator, MCC-135, which limits calcium overload, to mitigate reperfusion injury. They observed a similar increased release of troponin-I from both treated hearts and control hearts during reperfusion, a finding implying comparable damage to both groups of myocardia. The same reperfusion, however, caused a concomitant release of the myocardial-specific isoenzyme of creatine kinase (CK-MB) which was lower in the treated hearts than in the untreated hearts. This suggests that the MCC-135 saved some infarcted myocardium.

The molecular weight of troponin-I is 23 kDa and that of CK-MB, 86 kDa. In addition, troponin I is very susceptible to proteolysis in injured and necrotic cardiomyocytes. It is known that apoptotic cells and apoptotic bodies do not provoke inflammation because they do not release proteins into the extracellular space. It is also known that smaller molecules will penetrate injured plasma membranes more easily than larger molecules. On the basis of these facts, one can hypothesize that calcium modulator MCC-135 shifts cardiomyocyte death from oncosis to apoptosis, which is not favorable to a release of CK-MB. If this hypothesis is correct, the concomitant and serial use of cardiomyocyte markers of different molecular weights may become a method for an approximate evaluation of oncotic and apoptotic deaths in the heart.

Recently the effect of an anti-C5 complement antibody, applied as an adjunct to primary percutaneous coronary intervention, was studied [3]. Even though the antibody influenced clinical outcomes positively, it did not reduce infarct size as measured by release of CK-MB. It seems that the infarcts in the untreated hearts, being under the influence of complement [4], contained numerous apoptotic cardiomyocytes, which did not release macromolecular CK-MB into the circulation. Consequently, these infarcts appeared smaller than they really were.


   References
Top
 References
 

  1. Rizzuto R, Pinton P, Ferrari D, et al. Calcium and apoptosis: facts and hypotheses. Oncogene. 2003;22:8619–8627[Medline]
  2. Yarbrough WM, Mukherjee R, Escobar GP, et al. Modulation of calcium transport improves myocardial contractility and enzyme profiles after prolonged ischemia-reperfusion. Ann Thorac Surg. 2003;76:2054–2061[Abstract/Free Full Text]
  3. Beranek JT. Why did the anti-C5 complement antibody pexelizumab not reduce infarct size but influence clinical outcomes positively when applied as adjunctive therapy to primary percutaneous coronary intervention? Circulation. 2004;109:e195–e196[Free Full Text]
  4. Beranek JT. Why primary angioplasty is less offensive to the myocardium compared with thrombolysis for acute myocardial infarction. Am Heart J. 2000;140:e5

Related Article

MCC-135 Diminishes the Egress of CK-MB but Not of Troponin-I From Cardiomyocytes During Reperfusion: Reply
William M. Yarbrough and Francis G. Spinale
Ann. Thorac. Surg. 2005 79: 1095. [Extract] [Full Text] [PDF]




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