Serum creatine phosphokinase estimations in myocardial infarction.

Since the initial report on the clinical value of serum glutamic oxalacetic transaminase (SGOT) determinations in the diagnosis of myocardial infarction (LaDue, Wroblewski, and Karmen, 1954), a considerable amount of work has been done on the blood levels of other enzymes liberated from necrosed heart cells. Because of lack of specificity and difficulty of estimation, very few other enzyme estimations have been adopted as routine diagnostic tests. We have found the estimation of serum lactic dehydrogenase (SLD) to be a very useful supplementary test to SGOT determinations (Stewart and Warburton, 1961; King and Waind, 1960), a view not universally accepted, because raised SLD levels are found in a variety of conditions (Agress and Estrin, 1963). Latterly the specificity of the SLD estimation has been improved by making use of the different characteristics of lactic dehydrogenase of heart muscle origin, compared to that of other tissues. Thus, lactic dehydrogenase from heart muscle will respond differently to the effect of heat (Wroblewski and Gregory, 1961), to acetone precipitation (Latner and Turner, 1963), to chloroform inhibition (Warburton and Smith, 1963), in substrate specificity (Elliot and Wilkinson, 1961), and in electrophoretic mobility (Wroblewski, Gregory, and Ross, 1960a; Van der Helm et al., 1962). Since all these characteristics have been used to devise more specific tests for myocardial infarction, it is apparent that it is this lack of specificity that has caused most concern in accepting enzymological findings when cQnfirming a diagnosis of myocardial infarction. It has recently been shown that estimation of serum creatine phosphokinase (SCPK) may provide a very specific test for heart muscle necrosis (Dreyfus et al., 1960; Smith, 1964). This enzyme exhibits maximum activity in striated muscle, brain, and heart muscle, and is known to be liberated into the blood stream within a very short time following myocardial infarction, and subsequent heart muscle necrosis. It achieves a peak of maximum activity 18-30 hours from onset, and returns to normal after 3-4 days total increase. Since the involvement of brain and skeletal muscle produces symptoms so clinically different from myocardial infarction it appears that estimation of SCPK would prove an ideal test, providing it could be carried out on specimens collected within 3 days of onset.