Preconditioning has been described as the most potent form of protection against myocardial necrosis yet described (5). The protection conferred by preconditioning has been found against most of the deleterious effects induced by ischaemia and reperfusion, and in most animal models as well as in humans. While preconditioning undoubtedly delays infarct development, and offers intriguing mechanisms of endogenous protection, a word of caution is required before assuming that preconditioning could be the basis of a new-found therapy for patients. We attempt to take a critical look at the literature and to emphasise that the reduction of infarct size, often praised as an important consequence of preconditioning, has two important limitations. First, it is a delay in the development of necrosis that is achieved; thus preconditioning buys time but does not cheat death. Secondly, almost all the models used in the studies of infarct size reduction use regional ischaemia followed by reperfusion, so that the benefits of preconditioning could have occurred in either the ischaemic or in the reperfusion period, which is an important distinction. We will emphasise that preconditioning can have different end-points, and that not all of its effects are favourable. Specifically, there may be adverse effects during the ischaemic period, which differ from those on reperfusion.