Ever since it became apparent that anticoagulant therapy has no influence on the immediate course of coronary thrombosis, it has been tacitly assumed that the size of an infarct was determined by the initial injury and could not be altered through therapeutic intervention. Thus, attempts to improve coronary perfusion have been aimed not at preventing the spread of infarction, but at maintaining the function of the remaining healthy myocardium.
This fatalistic attitude has been challenged during the past decade by investigators who monitored aspects of infarction that had been hitherto unexplored. Changes in infarct size, as determined by electrocardiographic "mapping" combined with frequent measurements of serum creatine phosphokinase (CPK) level, and the effects of various types of intervention on the balance between myocardial oxygen demand and supply are discussed in two recent editorials by Braunwald1 and Braunwald and Maroko,2 investigators who have made noted contributions to this area
Vaisrub S. Shrinking the Myocardial Infarct. JAMA. 1974;230(9):1310–1311. doi:10.1001/jama.1974.03240090050030
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