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Ann Thorac Surg 2003;75:S656-S660
© 2003 The Society of Thoracic Surgeons

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I: Pathophysiology of ischemic-reperfusion injury

The basic biology of apoptosis and its implications for cardiac function and viability

^a Crafoord Laboratory of Experimental Surgery, Karolinska Hospital, Stockholm, Sweden

* Address reprint requests to Dr Valen, Crafoord Laboratory L6:00, Karolinska Hospital, 17176 Stockholm, Sweden.
e-mail: guro.valen{at}cmm.ki.se

Presented at the 3^rd International Symposium on Myocardial Protection From Surgical Ischemic-Reperfusion Injury, Asheville, NC, June 2–6, 2002.

Abstract

Apoptosis or programed cell death is a continuous process of destruction of nonfunctional cells. It is a physiologic process whereby the body disposes of unwanted cells by self-destruction and is our utmost defense against damaged cells. There are several pathways leading to programed cell death. Apoptosis is seen in failing, infarcted, and hibernating human hearts, and during open heart surgery. Apoptosis appears to be induced by myocardial ischemia-reperfusion injury and this is reduced by ischemic preconditioning. Antiapoptotic interventions may be a future target for myocardial protection.

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