Creatine kinase (CK) and its isoenzyme CK-MB are important tools for the diagnosis of acute myocardial infarction. The content of CK-MB relative to total CK in myocardial cells is variable; it is low in normal myocardium and increased several-fold in hypoxic myocardium. We tested the hypothesis that CK-MB mass (CK-MBm) could be related to cardiovascular history, preinfarctional medication and clinical course during myocardial infarction. In a prospective study CK and CK-MBm were measured 0, 6, 12, 18, 24, 36, 48 and 72 h after the admission to the coronary care unit. Peak values and areas under the curve (AUC) were determined and normalized for total CK activity (CK-MBm/CK). Of 185 patients with acute chest pain, 70 patients had 71 acute myocardial infarctions and were enrolled in the study. A history of chronic angina pectoris or hypertension had no influence on CK-MBm/CK levels. In contrast, treatment with beta-blockers before infarction resulted in a lower relative CK-MBm peak value (CK-MBm/CK 6.0 (median value), range 3.1-15.3, versus 7.0, range 0.5-17.3: p < 0.05). Other drugs had no influence. Patients with persistent pain on admission tended to have higher relative CK-MBm values (peak CK-MBm/CK: 6.8, range 0.5-17.3, versus 5.3, range 1.4-7.9, p = 0.08; AUC CK-MBm/CK: 0.05, range 0.01-0.10, versus 0.03, range 0.01-0.06, p < 0.05). Three vessel disease on coronary angiography was associated with higher peak CK-MBm/CK values during the acute phase of myocardial infarction than those with 1-2 vessel disease (Peak CK-MBm/CK: 7.9, range 5.5-17.3, versus 6.4, range 3.1-10.2, p < 0.05; AUC CK-MBm/CK: 0.06, range 0.02-0.11, versus 0.04, range 0.02-0.07, p < 0.05). We conclude that relative CK-MBm/CK levels reflect to a certain degree the extent of the coronary disease and that preinfarctional beta-blockade may result in lower CK-MBm levels.