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Ann Thorac Surg 2004;77:1689-1690
© 2004 The Society of Thoracic Surgeons

Invited commentary

^b UCI Medical Center, 101 The City Drive Bldg 53, Rt 81, Orange, CA 92868-4080 USA
^a Division of Cardiology, VA Medical Center and University of Minnesota, Minneapolis, MN 55417 USA

e-mail: shekh003@tc.umn.edu
e-mail: narula@uci.edu

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This study by Mukherjee et al is provocative and has a high potential for therapeutic utility. Consistent with other Pdata, they found that myocytes exposed to simulated hypothermic hyperkalemic cardioplegic arrest (HCA) demonstrated contractile dysfunction. More interestingly, they also found that a significant portion of this dysfunction could be attenuated with nonspecific caspase inhibition. This paper adds to the growing body of evidence that caspases play a role in myocardial dysfunction. Caspase over expression results in cardiac dysfunction [1, 2], while inhibiting caspase activity ameliorates this dysfunction [2, 3]. While some of . . . [Full Text of this Article]