The term preconditioning was applied to the observation made in 1986 by Mur
ry and colleagues that canine myocardium subjected to brief episodes of isc
hemia and reperfusion would tolerate a more prolonged episode of ischemia b
etter than myocardium not previously exposed to ischemia. Since that semina
l observation, protective effect of preconditioning was demonstrated in all
animal species tested, resulting in the strongest form of in vivo protecti
on against myocardial injury other than early reperfusion. Angina heralding
acute myocardial infarction may represent the clinical correlate of precon
ditioning phenomenon in humans. Data from small pathophysiological studies
demonstrated that prodromal angina (<48 hours prior to index myocardial inf
arction) causes a reduction of infarct size and consequently a better left
ventricular function compared with patients without such clinical feature b
efore myocardial infarction. The protective effect of prodromal angina was
also confirmed in larger prospective studies; its presence translates into
a significant reduction of a combination of death, cardiogenic shock and pu
lmonary edema during hospital stay. The exact mechanism of such clinical ph
enomenon is however not known, but it may include preconditioning. Other me
chanisms have been also claimed to play an important role, like a more rapi
d lysis of the occlusive thrombus within the infarct-related artery, or a r
apid opening of intramural collateral not visible at angiography. Whatever
the mechanism, it appears that patients with prodromal angina before myocar
dial infarction exhibit, when rapidly reperfused, a better post-infarction
clinical outcome. At the present "optimal preconditioning-mimetic agents" a
re yet to be found, and "putting preconditioning in a bottle" still remains
a pharmacologic challenge. (C) 1999 Elsevier Science Ireland Ltd. All righ
ts reserved.