A brief ischemic episode (ischemic preconditioning) limits myocardial
necrosis produced by a prolonged period of coronary artery occlusion a
nd reperfusion. In absence of infarction, lack of cumulative ATP deple
tion, and ventricular arrhythmias and dysfunction ''stunning'' in mode
ls of intermittent ischemia and reperfusion also could be a component
of an adaptive response to brief ischemia (preconditioning). Nonischem
ic stimuli also precondition the myocardium against ventricular arrhyt
hmias and infarction by activating endogenous mechanism(s) of protecti
on similar to that induced by ischemic preconditioning. Preservation o
f myocardial ATP, abolishing purine release, attenuation of free radic
al production, activation of adenosine receptors and K-ATP channels, a
nd induction of heat shock proteins are common responses to ischemic a
nd nonischemic stimuli of preconditioning. Although a significant redu
ction in myocardial infarction is critical to myocardial salvage and p
atient survival, it is equally important to have a functioning heart t
hat 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 i
nclude nonischemic stimuli of preconditioning and other important moni
tors of myocardial protection such as ventricular function and electro
physiological stability in addition to that of infarction.