Abstract
The possibility that the heart may be rendered more resistant to the damaging effects of ischaemia-reperfusion injury is an attractive therapeutic goal. In the developed world, coronary heart disease now constitutes the most important independent cause of mortality. The treatment of myocardial infarction has been revolutionised by the use of thrombolytic agents which, if administered early, will frequently allow reperfusion and limit the size of the infarct. However, the benefit in terms of improved mortality diminishes rapidly if treatment is delayed. Endogenous mechanisms of myocardial protection provide a possible means by which the progress of myocardial necrosis might be slowed, increasing the time available for effective reperfusion. Similar considerations apply in patients with unstable angina and in those undergoing coronary artery surgery. Improved myocardial protection may also assist the preservation of explanted hearts prior to transplantation. A more detailed understanding of the cellular mechanisms involved in mediating cytoprotection may allow future development of pharmacological agents capable of invoking persistent protection against myocardial ischaemia.