The diagnosis of myocardial infarction using cardiac-specific isoenzyme profiles

Abstract

Creatine kinase (CK) and lactate dehydrogenase (LD) isoenzyme activities were measured in 100 patients with suspected acute myocardial infarction (AMI). The method employed was electrophoresis on thin agarose films using the Corning-ACl apparatus and reagents. The usefulness of this procedure as an aid to diagnosis and management was assessed. Specimens were collected at critical times on the enzyme release curve, the first on admission, then at intervals of 6-13 and 24-37 h. A comparison was made using significant elevations in total CK and α-Hydroxybutyrate dehydrogenase (α-HBDH) activities on specimens collected as part of the daily routine. In 34 patients there was an excellent correlation between both methods of analysis. However, the isoenzyme profile provided confirmation of AMI in a further 7 patients. In these patients total CK remained within the reference range (<80 μ 1) or showed borderline increases (80-160 μ/l), although α-HBDH remained normal. Among the remaining 48 patients in which AMI was ruled out. 4 showed elevations in total CK due to non-cardiac conditions. In a further 2 patients, in which total CK remained normal, trace amounts of CK-MB were detected. Both of these patients suffered episodes of atrial fibrillation. The individual assays for each collection period revealed that 61%, of the specimens were positive for CK-MB on the admission sample, whereas 93% were positive by the second specimen. However elevations in total CK ( > 160 μ/l) occurred in only 24% of patients on the first specimen, whereas 68%, were elevated by the second. The ratio of LD1:LD2> 1 occurred in 20% on admission but 85%, by 24-37 h. This coincided with α-HBDH being elevated in 24%, and 78% of patients respectively. Therefore, the combination of CK and LD isoenzyme profiles provided a more rapid and specific indication of AMI. Creatine kinase (CK) and lactate dehydrogenase (LD) isoenzyme activities were measured in 100 patients with suspected acute myocardial infarction (AMI). The method employed was electrophoresis on thin agarose films using the Corning-ACl apparatus and reagents. The usefulness of this procedure as an aid to diagnosis and management was assessed. Specimens were collected at critical times on the enzyme release curve, the first on admission, then at intervals of 6-13 and 24-37 h. A comparison was made using significant elevations in total CK and α-Hydroxybutyrate dehydrogenase (α-HBDH) activities on specimens collected as part of the daily routine. In 34 patients there was an excellent correlation between both methods of analysis. However, the isoenzyme profile provided confirmation of AMI in a further 7 patients. In these patients total CK remained within the reference range (<80 μ 1) or showed borderline increases (80-160 μ/l), although α-HBDH remained normal. Among the remaining 48 patients in which AMI was ruled out. 4 showed elevations in total CK due to non-cardiac conditions. In a further 2 patients, in which total CK remained normal, trace amounts of CK-MB were detected. Both of these patients suffered episodes of atrial fibrillation. The individual assays for each collection period revealed that 61%, of the specimens were positive for CK-MB on the admission sample, whereas 93% were positive by the second specimen. However elevations in total CK ( > 160 μ/l) occurred in only 24% of patients on the first specimen, whereas 68%, were elevated by the second. The ratio of LD1:LD2> 1 occurred in 20% on admission but 85%, by 24-37 h. This coincided with α-HBDH being elevated in 24%, and 78% of patients respectively. Therefore, the combination of CK and LD isoenzyme profiles provided a more rapid and specific indication of AMI.