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M yocardial ischemia is commonly associated withcoronary artery disease as well as many congenital and acquired heart diseases without obstructed coronary arteries. With brief ischemia ventricular function is impaired but myocytes recover, whereas prolonged ischemia causes necrosis and associated fibrosis. Necrosis may be confluent, as in complete obstruction of a branch coronary artery, or patchy, as with intermittent decreases of regional blood flow, for example in aortic stenosis. These ischemic changes are predominantly subendocardial in either ventricle.1,2 Once assessed by an appropriately designed study, knowledge of whether these ischemic changes are likely might be useful in determining the timing of surgery, for example, deciding when to replace an aortic valve. It seems reasonable to repair the lesion before permanent myocardial damage has occurred.
Hoffman et al. (Wed,) studied this question.