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Ann Thorac Surg 2002;73:1235
© 2002 The Society of Thoracic Surgeons
Department of Surgery, Hospital of the University of Pennsylvania, 3400 Spruce St, Philadelphia, PA 19104, USA
e-mail: gormanr{at}uphs.upenn.edu
Myocardial stunning is defined as a reversible contractile impairment that is induced by a period of ischemia followed by reperfusion [1]. The mechanism of myocardial stunning remains incompletely elucidated. A better understanding of this phenomenon has important implication for myocardial protection, organ preservation, reperfusion of myocardial infarctions and ventricular remodeling.
Apoptosis is an energy dependent form of cell death that is distinct from necrosis. Initially, it was believed that apoptosis did not occur in terminally differentiated cells such as cardiac myocytes [2]. The discovery that myocyte apoptosis was present to a significant degree in some patients with end-stage cardiomyopathy [3] has provided an impetus for further research into the role of apoptosis in a variety of cardiac disorders. Although there is relatively scant evidence in the literature linking myocyte apoptosis to the pathophysiogy of stunned myocardium [4] such a hypothesis is intriguing since both phenomenon are associated with the generation of reactive oxygen species [5] and alteration in cellular calcium homeostasis [6].
Doctor Schmitt and colleagues in this preliminary, but interesting study, have demonstrated histologic, histochemical, and biochemical evidence of myocyte apoptosis in a group of patients who underwent coronary artery bypass grafting. The authors also found a direct correlation between the degree of myocyte apoptosis and both aortic occlusion time and myocardial stunning. All operations were performed using cardiopulmonary bypass, aortic cross clamping and an accepted myocardial preservation strategy. All patients had normal cardiac function prior to the operation.
This article is important for three reasons. First, the data demonstrate that the TUNEL method is a relatively insensitive assessment of the degree of myocyte apoptosis. This assay only becomes positive in the terminal stages of the apoptotic pathway when DNA fragmentation becomes significant. Narula and associates have clearly shown that caspase induced cytosolic myofibrillarlysis may proceed to a dramatic extent in cells in which DNA fragmentation never develops. They have termed these cells myofibrillarlytic or zombie myocytes. Why these cells do not complete the apoptotic pathway remains an open area of investigation [7]. Second, if myocyte apoptosis is confirmed as a significant contributor to the contractile dysfunction of stunned myocardium it would provide a therapeutic target for improving the results of intraoperative myocardial protection, preservation of donor hearts, and percutaneous revascularization of myocardial infarction. Third and most importantly, the transient nature of myocardial stunning would imply that reperfusion induced myocyte apoptosis is at least a partially reversible process. Elucidation of how the apoptotic cascade is reversed would provide valuable information for treating other cardiac disorders that have been associated with myocyte apoptosis such atherosclerosis and postinfarction ventricular remodeling.
References
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  J. P. Schmitt and H. Aebert Reply Ann. Thorac. Surg., January 1, 2004; 77(1): 382 - 382. [Full Text] [PDF]
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