Numerous reports suggest that stress protein accumulation confers protection in various mammalian tissues against differing stresses. The purpose of this article is to review the evidence that stress proteins, in particular hsp70, are able to alter the resistance of the heart to subsequent ischaemic and non-ischaemic injury and to discuss the possible physiological basis for this apparent protection. The possible, though unlikely involvement of heat stress proteins in classical ischaemic preconditioning is addressed as is the possibility of their involvement in a delayed second window of protection.