Abstract
Infarct size has been estimated from serial serum creatine phosphokinase (CPK) changes, but the contribution of noncardiac CPK may interfere. Results would also be influenced if CPK disappearance varied with hemodynamic changes. Since MB CPK is a marker more specific to myocardium, infarct size was estimated from serum MB changes in 16 patients. In addition, 21 chronically instrumented conscious dogs subjected to tachycardia, decreased cardiac output or hepatic or renal ischemia were studied to evaluate the dependence of CPK disappearance on hemodynamics. MB CPK in human tissue extracts and serum was quantified with a new, rapid, glass bead batch adsorption technique, verified wth CPK isoenzymes prepared from human myocardium. Among tissues surveyed, only myocardium contained appreciable MB CPK. Infarct size estimated from MB correlated with total serum CPK in patients with uncomplicated myocardial infarction (r = 0.97, N = 12). In patients with infarction given intramuscular injections, total CPK curves were distorted but MB CPK curves were not apparently affected. Hemodynamic alterations in conscious dogs did not markedly affect the disappearance rate (kd) of intravenously injected, radioactively labeled, canine myocardial CPK, although kd was shown to depend on reticuloendothelial system activity. These findings suggest that estimation of the extent of infarction based on serum MB CPK should be useful despite hemodynamic deterioration associated with infarction or interference of noncardiac CPK.