The severity of myocardial damage appears to be a common denominator contributing to electrophysiologic derangements, impaired ventricular function, and prognosis after myocardial infarction. Physiologically based models of processes affecting appearance and disappearance of CPK from the circulation may improve predictions and estimates of infarct size. Elevation of serum MB CPK isoenzyme activity appears to be a highly sensitive and specific indicator of myocardial injury. Despite the limitations discussed, recently developed enzymatic methods for detection, projection, and quantification of infarct dize have demonstrated that the extent of myocardial injury may be limited in selected patients by appropriate therapeutic measures. Further investigation may help to define the intervals between the onset of infarction and implementation of therapeutic maneuvers during which myocardial protection is possible, and may help to identify and differentiate inter ventions which salvage myocardium, those which improve cardiac performance without altering infarct size, and those which augment cardiac injury despite improving hemodynamics. Thus, in conjunction with electrophysiologic, radioisotopic, and hemodynamic techniques, enzymatic estimates and projection of infarct size should facilitate increased understanding of factors influencing the evolution of infarction and hasten development of effective therapeutic interventions designed to reduce myocardial damage.