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Creatine kinase and creatine kinase B‐subunit in stable and unstable angina pectoris

Abstract. Repetitive ischaemic episodes may have a cumulative effect leading to irreversible myocardial cell damage with enzyme release. Using plasma creatine kinase (CK) and creatine kinase B‐subunit (CK‐B) concentrations this theory has been tested in forty‐eight patients admitted with acute chest pain, but without ECG signs of acute myocardial infarction (AMI). The patients were classified into four groups: Fourteen patients with non‐ischaemic heart disease (non‐IHD), seventeen with stable angina pectoris (SAP), ten with unstable angina pectoris (UAP), and seven patients who developd AMI during the study period. The enzyme variation in non‐IHD delineates the background noise, and the increased variability in AMI indicates the full scale of the enzyme signals in cases of irreversible cell damage. Patients with SAP have the same enzyme signal as the background noise in respect of both CK and CK‐B. However, in UAP the signal of CK‐B equals the background noise, whereas the CK signal is separated from the latter. The reason may be that the signal to noise ratio of CK‐B is poor and the analytical sensitivity low. Therefore, the behaviour of CK‐B in this study does not support the above theory although our findings for CK indicate that the consequence of repeated ischaemic attacks is slight enzyme release.