(Circulation. 1999;100:559-563.)
© 1999 American Heart Association, Inc.
Current Perspective |
From the Divisione di Cardiochirurgia, Università di Roma Tor Vergata, European Hospital and Istituto di Cardiologia (F.C.), Università Cattolica del Sacro Cuore, Rome, Italy.
Correspondence to Dr Fabrizio Tomai, Divisione di Cardiochirurgia, Università di Roma Tor Vergata, European Hospital, via Portuense 700, 00149 Rome, Italy.
AbstractIschemic
preconditioning, a powerful form of endogenous protection
against myocardial infarction, has been demonstrated in several animal
species and, recently, in isolated human cardiomyocytes.
For both logistic and ethical reasons, no clinical study can meet the
strict conditions of experimental studies on preconditioning with
infarct size as the end-point. Nevertheless, the demonstration of
adaptation to ischemia observed during in vitro studies on
human atrial trabeculae, in patients in the setting of
coronary bypass surgery, and in the setting of coronary
angioplasty in the absence of collateral vessel recruitment strongly
suggests that ischemic preconditioning occurs in humans. This
notion is further supported by the observation that in these human
models, the adaptation to ischemia is influenced by drugs
acting on KATP channels and on purinergic and
-adrenergic receptors, similar to what is observed in accepted
experimental models of ischemic preconditioning. This important
form of myocardial endogenous protection may also play a
role in the warm-up phenomenon and in mediating the beneficial effects
of preinfarction angina. The demonstration of ischemic
preconditioning in humans and the identification of some of its
mediators suggests that in patients at high risk for myocardial
infarction, drugs known to block this endogenous form of
protection should be used with caution, whereas drugs known to elicit
preconditioning might have a relevant therapeutic role.
Key Words: angina ischemia myocardial infarction
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