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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: Reply

William M. Yarbrough, MD, Francis G. Spinale, MD, PhD

Division of Cardiothoracic Surgery, Strom Thurmond Research Building, Medical University of South Carolina, 114 Doughty St, Charleston, SC 29425, USA

wilburnm{at}musc.edu

To the Editor:

We extend our appreciation to Dr Beranek for his comments on and interest in our recent investigation using the calcium modulating agent MCC-135 [1]. In this study, we demonstrated that MCC-135 modified the degree of myocardial injury with respect to the release of the myocardial-specific isoenzyme of creatine kinase. However, it remained unclear whether the degree of myocyte injury in this model of ischemia and reperfusion was due to changes in the degree of necrosis, oncosis, or apoptosis. It is possible that the deployment of MCC-135 in the context of ischemia and reperfusion modified calcium-sensitive intracellular proteolytic pathways, which would, in turn, alter the portfolio of molecules released from the myocyte.

As suggested by Dr Beranek, one approach to address this issue is through measuring multiple markers of different molecular weights in this model of ischemia plus reperfusion. This would allow an answer to the hypothesis he posed, ie, that perhaps distinct serum markers of myocardial injury can be used to facilitate the evaluation of oncotic and apoptotic myocyte death after ischemia and reperfusion.

Thus, although our study was one of the first to temporally profile release of myocyte-specific enzymes in a clinically relevant model of ischemia and reperfusion, future studies that more carefully address the mechanism by which MCC-135 afforded myocardial protection are warranted. One approach would be to use an isolated myocyte system of ischemia and reperfusion or, more relevant to the cardiac surgical setting, an isolated myocyte system of cardioplegic arrest [2]. This isolated system would provide a means to more carefully examine intracellular processes that may be modified by MCC-135 and the mechanisms by which these processes would alter the progression to oncosis or apoptosis. This approach may also be amenable to address Dr Beranek's reference to a strategy involving an anti-C5 complement antibody.

Future studies are certainly warranted, but our past investigation and the comments of Dr Beranek emphasize the importance of evaluating cardiac enzyme release in the context of the experimental or clinical condition. It is hoped that the outcome of these studies will be a more focused strategy to prevent myocyte death with ischemia-reperfusion injury and that the study with MCC-135 will provide the stimulus for more mechanism-based studies, that can eventually be translated into clinical practice.


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 References
 

  1. 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]
  2. Dorman B, Hebbar L, Zellner JL, et al. ATP-sensitive potassium channel activation before cardioplegia: effects on ventricular and myocyte function. Circulation. 1998;98(Suppl 2):176–183

Related Article

MCC-135 Diminishes the Egress of CK-MB but Not of Troponin-I From Cardiomyocytes During Reperfusion
Jiri T. Beranek
Ann. Thorac. Surg. 2005 79: 1095. [Extract] [Full Text] [PDF]




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