Enzymatic estimation of infarct size during reperfusion.

Infarct size estimated enzymatically is an objective end point for assessing interventions in patients with acute myocardial infarction and correlates with acute and long-term morbidity and mortality. However, there is concern whether such estimates are reliable in the setting of reperfusion. Reperfusion during experimental infarction and clinically with streptokinase is associated with higher plasma creatine kinase (CK) levels that peak much earlier than with sustained occlusion, indicating a more rapid release rate. In this report, experimental derivation of the parameters for estimating infarct size--myocardial CK distribution and content, CK depletion, plasma CK disappearance rate and the release ratio--are presented, together with the experimental and clinical validation of these estimates. The close correlation between myocardial CK depletion and morphometric estimates of infarct size (r = .92), which provides the basis for enzymatic estimation of infarct size, remains valid during experimental reperfusion. Plasma CK activity (100-5000 IU/l) assayed before and after incubation of streptokinase (5000 U/ml for 30 minutes at 37 degrees C) showed less than 5% variation. Plasma CK disappearance (kd) in the conscious dog before and during infusion of streptokinase (20,000 U/hour) were identical. The CK release ratio has not been determined during streptokinase therapy or experimental reperfusion, but in the experimental animal during early reperfusion, infarct size was overestimated by the plasma CK method compared with histologic estimates. Despite the overestimation, enzymatic estimates still correlate closely with histologic estimates (r = .90). The presence of a close correlation despite sudden complete early restoration of flow suggests that with the appropriate experimentally determined correction factors, one can obtain reliable enzymatic estimates of infarct size to assess the efficacy of streptokinase.