Serum CK-MB in Diagnosis and Assessment of Acute Myocardial Infarction

  • Richard D. White
  • Peer Grande
  • Galen S. Wagner


When coronary care units were first developed in the early 1960s, it became important to make a prompt diagnosis regarding presence or absence of an acute myocardial infarct (AMI) to optimize the use of these specialized facilities. This diagnosis was extremely difficult when no new Q waves appeared on the electrocardiogram (ECG) during the first 24–48 h following CCU admission. Total “cardiac” enzyme determinations were an alternative, and when glutamic oxaloacetic transaminase (SGOT), lactic dehydrogenase (LDH), and creatine kinase (CK) all remained within normal limits, the diagnosis of an acute infarct was excluded. However, a variety of other body tissues could be the source of transient elevations of each of these enzymes. The first attempt to specifically identify the tissue of origin of an enzyme was the electrophoretic method for separating the isoenzymes of LDH [1]. This improvement over the use of total LDH was still suboptimal, because (a) an elevation in LDH1 could result from hemolysis as well as from myocardial necrosis, and (b) the results were expressed as ratios of one isoenzyme (LDH1) to another (LDH2) rather than the absolute level of a particular isoenzyme.


Acute Myocardial Infarction Creatine Kinase Infarct Size Myocardial Infarct Size Acute Myocardial Infarc 
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Copyright information

© Martinus Nijhoff Publishing, Boston/Dordrecht/Lancaster 1985

Authors and Affiliations

  • Richard D. White
  • Peer Grande
  • Galen S. Wagner

There are no affiliations available

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