Experimental Cardiology, Thoraxcenter,
Erasmus University Rotterdam,
Rotterdam, The Netherlands
To the Editor:
The clinical existence and relevance of ischemic
preconditioning will remain difficult to prove because patients cannot
be subjected to the rigorous protocols performed in laboratory animals
and because of our inability to accurately determine infarct size and
its determinants in humans. Furthermore, the presence of
atherosclerotic lesions in coronary arteries can result in
intermittent/chronic ischemia that could result in tolerance to
the ischemic stimulus.1 Consequently,
investigating the phenomenon of ischemic preconditioning in
animal models that mimic the clinical situation is important. It was
therefore with great interest that we read the article by Kapadia et
al2 in which they describe that the protective
effect of ischemic preconditioning is not abolished in the
presence of a critical stenosis. Although this study in a
closed chest swine model is another major step forward in bridging the
gap between the laboratory and the clinical setting, there are a number
of issues that deserve comment.
The authors did not find a protective effect of the
stenosis alone, which reduced blood flow by approximately 35%
(P=NS), and indicated that this finding is at variance with
the results of a study from our laboratory in which we showed that
30-minute 70% flow reduction resulted in a reduction of infarct size
produced by 60 minutes of coronary artery
occlusion.3 However, in a subsequent
study4 we demonstrated that when flow was reduced
by only 30% for up to 90 minutes immediately preceding the 60 minutes
of total coronary occlusion, cardioprotection was absent.
Furthermore,
Department of Medicine,
Rhode Island Hospital,
Providence, RI
Richmond, Va
© 1998 American Heart Association, Inc.
Correspondence
Effects of Ischemic Preconditioning
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