Heat stress preconditioning and delayed myocardial protection: what is new?

As other preconditioning phenomena, heat stress is able to induce a delayed myocardial protection against ischaemia-reperfusion injury by preserving ventricular function, preventing arrhythmia occurrence and reducing cellular necrosis. The development of heat stress response has been extensively studied in order to characterize the different steps of this form of preconditioning. It appears that chemical signals (such as nitric oxide, reactive oxygen species (ROS)) released by sublethal hyperthermic stress trigger a complex cascade of signalling events that include activation of protein kinase C (PKC) and mitogen-activated protein kinases (MAPK) and culminate in increased synthesis of inducible nitric oxide synthase, cyclooxygenase-2, antioxidant enzymes and protective proteins such as heat stress proteins (Hsps). A better understanding of this powerful protective adaptation of the cardiomyocyte is essential for the development of clinical applications and the design of cardioprotective pharmacological agents. The purpose of this letter is to review current information regarding the characteristics of heat stress preconditioning compared to other forms of late preconditioning.