Acute coronary occlusion is the leading cause of morbidity and mortality in the Western world, and according to the World Health Organisation will be the major cause of death in the world as a whole by the year 2020.1 Although the management of this epidemic will centre on the development of effective primary prevention programmes, the impact of these strategies may be limited, particularly in the developing countries. There is an urgent need for effective forms of secondary prevention and, in particular, treatments which will limit the extent of an evolving myocardial infarction during the acute phase of coronary occlusion—the death of myocardium represents a catastrophic event since dead myocytes are not replaced by division of surviving myocytes. Preserving the viability of ischaemic myocardium therefore presents a therapeutic target. Although appreciated for many years, this concept has so far failed to produce a clinically useful agent capable of protecting the ischaemic myocardium from infarction. The term “cardioprotection” has been used loosely during the last few decades to describe various therapeutic approaches, including antiarrhythmic, antianginal, antihypertensive, and antiplatelet treatments. In the present discussion, we apply the term “cardioprotection” very specifically to describe interventions that preserve or enhance the viability of myocardium during ischaemia and reperfusion and thus limit the extent of acute myocardial infarction. It is our contention that in the light of current understanding of the mechanisms of cell injury during both ischaemia and reperfusion, we are well placed to identify molecular targets which may provide the foundation on which rational therapeutic approaches can be based.