The recognition of acute myocardial infarction in the past has depended on certain electrocardiogram and cardiac enzyme alterations in association with a particular clinical history. However, in certain instances these parameters are not sufficient to either make a positive diagnosis of acute myocardial infarction or to exclude its presence. In particular, the presence of left bundle branch block, previous myocardial infarction and recent cardioversion all provide certain difficulties as far as the electrocardiographic recognition of acute myocardial infarction is concerned. Moreover, subendocardial myocardial infarction can never be precisely identified from the electrocardiogram alone; this is a matter of some concern since the subendo-cardium is the area most vulnerable to ischemic damage in experimental animals (1-3). In general, cardiac enzyme abnormalities are not so specific for myocardial damage that enzyme elevations in any individual patient might not be due to congestive heart failure, hemolysis, brain or pulmonary damage, intramuscular injection, etc., although the recent studies utilizing the myocardial specific creatine phosphokinase isoenzyme have suggested that it may be of more value in the exact recognition of myocardial infarction than the others (4).