Myocardial Preconditioning: A Model or a Phenomenon?

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A brief ischemic episode (ischemic preconditioning) limits myocardial necrosis produced by a prolonged period of coronary artery occlusion and reperfusion. In absence of infarction, lack of cumulative ATP depletion, and ventricular arrhythmias and dysfunction "stunning" in models of intermittent ischemia and reperfusion also could be a component of an adaptive response to brief ischemia (preconditioning). Nonischemic stimuli also precondition the myocardium against ventricular arrhythmias and infarction by activating endogenous mechanism(s) of protection similar to that induced by ischemic preconditioning. Preservation of myocardial ATP, abolishing purine release, attenuation of free radical production, activation of adenosine receptors and KATP channels, and induction of heat shock proteins are common responses to ischemic and nonischemic stimuli of preconditioning. Although a significant reduction in myocardial infarction is critical to myocardial salvage and patient survival, it is equally important to have a functioning heart that can sustain systemic pressure without inotropic support or assist devices. It is scientifically challenging and clinically important to elucidate the mechanisms of myocardial preconditioning. However, it is necessary to expand the definition of myocardial preconditioning to include nonischemic stimuli of preconditioning and other important monitors of myocardial protection such as ventricular function and electrophysiological stability in addition to that of infarction.