Circulation, Vol 66, 1146-1149, Copyright © 1982 by American Heart Association
E Braunwald and RA Kloner
Myocardial ischemia has, for many decades, been viewed as an all-or- none
process that causes myocardial necrosis when prolonged and severe, but
whose effects are transient when it is brief or mild. In view of the
evidence that the ischemic process may "hit, run and stun," perhaps our
thinking about the consequences of myocardial ischemia should be expanded.
According to this formulation, an ischemic insult not of sufficient
severity of duration to produce myocardial necrosis may acutely affect
myocardial repolarization and cause angina (hit); but these changes wane
rapidly (run), when the balance between myocardial oxygen supply and demand
has been reestablished. However, the ischemia may interfere with normal
myocardial function, biochemical processes and ultrastructure for prolonged
periods (stun). The severity and duration of these postischemic changes
depend on the length and intensity of the ischemia, as well as on the
condition of the myocardium at the onset of the ischemic episode.
Furthermore, it is likely that when the myocardium is repeatedly stunned,
it may exhibit chronic postischemic left ventricular dysfunction, an
ill-defined condition. If prolonged, chronic postischemic left ventricular
dysfunction can progress to myocardial scarring and ischemic
cardiomyopathy, it may be important to determine how often it can be
ameliorated by permanent improvement of myocardial perfusion by surgical
treatment.
ARTICLES
The stunned myocardium: prolonged, postischemic ventricular dysfunction
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