Abstract
Results of estimation of infarct size with a selected biochemical marker in blood, creatine phosphokinase (CPK), have suggested that infarct size is an important determinant of prognosis, impaired ventricular function, early ventricular dysrhythmia, and the severity of clinical manifestations. Estimates based on serial changes in serum CPK activity have correlated closely with morphological estimates and have been employed to evaluate therapeutic interventions. Improved estimates with any biochemical marker require exclusion of noncardiac sources of the marker and characterization of the influence of physiological alterations on parameters in empirical or physiologically based mathematical models utilized. Use of MB CPK instead of total CPK therefore improves enzymatic estimates when infarction is accompanied by release of noncardiac CPK into the circulation. Preliminary results with physiologically based models of CPK release from the infarct and its disappearance from the circulation suggest that release may be diffusion limited and that the CPK disappearance rate is relatively uninfluenced by profound hemodynamic derangements or myocardial infarction per se. The substantial inactivation of CPK in lymph in vitro and in situ underscores the importance of defining factors influencing the proportion of a biochemical marker depleted from necrotic myocardium appearing in blood, since the proportion is one parameter used in models employed to quantitatively estimate irreversible ischemic injury.