Heat Stress Proteins and Their Relationship to Myocardial Protection

Acute myocardial infarction is the most common cause of death in men in the Western world. The treatment of this condition is no longer simply supportive, awaiting the complications of ischaemic injury, but has entered a new era where the mortality of acute myocardial infarction can be approximately halved by thrombolytic agents and aspirin (ISIS-2 1988), with the greatest benefit seen in those treated soon after the onset of symptoms. The lack of a reduction in mortality when thrombolytic treatment is administered late is most likely due to the fact that the prolonged coronary occlusion has resulted in such severe necrosis of the myocardium that little benefit can be derived by restoring blood flow (Reimer and Jennings 1979). Therefore any intervention that could delay the onset of tissue necrosis could buy valuable time by extending the effective temporal window for thrombolysis. Attempts to limit myocardial infarct size over the last decade with exogenous pharmacological agents have been largely unsuccessful (Hearse and Yellon 1983), prompting us and others to explore the heart’s endogenous protective mechanisms to ascertain if this route may provide us with the knowledge required to protect the myocardium from severe ischaemic injury.