Diagnostic changes in plasma creatine kinase isoforms early after the onset of acute myocardial infarction

Allan S Jaffe, H. Serota, A. Grace, B. E. Sobel

Research output: Contribution to journalArticle

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Abstract

Conventional plasma isoenzyme and enzyme values usually are normal during the first few hours of acute myocardial infarction. Thus definitive diagnosis may be delayed. We have shown recently that infarction in dogs can be detected within 1 hr after coronary occlusion by analysis of relative activities of MM creatine kinase (CK) isoforms in plasma. Isoforms of MM CK evolve through posttranslational modifications in plasma of the form released from tissue (MM(A)) to MM(B) and MM(C). In this study we quantified changes in isoform profiles in the first available plasma samples from patients with evolving myocardial infarction, from patients with angina, and from normal subjects. In the 26 control subjects, the ratio of MM(A) to MM(C) was 1.09 ± 0.45 (SE) (range 0.31 to 3.1; upper limit of normal [defined as the mean plus 2 SD] 2.5). In the seven control patients with coronary artery disease, the ratio of MM(A) to MM(C) was 1.3 ± 0.3 with a range of 0.5 to 2.5. In contrast, among the 28 patients with acute myocardial infarction, the ratio of MM(A) to MM(C) in the first available plasma sample averaged 14.6 ± 4.5 (p < .01 compared with both control groups). First available samples were obtained 3.9 ± 0.4 hr after the onset of pain. In 24 of 28 patients (86%) the ratio of MM(A) to MM(C) was greater than 2.5. Thus unequivocal changes in isoform profiles were evident in samples in which total and MB CK were within normal limits (79.7 ± 6.2 IU/liter for total CK and 4.4 ± 0.4 IU/liter for MB CK in patients with infarction compared with 90 ± 6.5 and 68 ± 11 IU/liter for total CK and 4.5 ± 0.4 and 4 ± 0.8 IU/liter for MB CK in normal control subjects and patients with angina, respectively). Accordingly, diagnostic changes in CK isoform profiles occur early after the onset of acute myocardial infarction.

Original languageEnglish (US)
Pages (from-to)105-109
Number of pages5
JournalCirculation
Volume74
Issue number1
StatePublished - 1986
Externally publishedYes

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Creatine Kinase
Protein Isoforms
Myocardial Infarction
MB Form Creatine Kinase
MM Form Creatine Kinase
Infarction
Coronary Occlusion
Post Translational Protein Processing
Isoenzymes
Coronary Artery Disease
Reference Values
Dogs
Pain
Control Groups
Enzymes

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine

Cite this

Diagnostic changes in plasma creatine kinase isoforms early after the onset of acute myocardial infarction. / Jaffe, Allan S; Serota, H.; Grace, A.; Sobel, B. E.

In: Circulation, Vol. 74, No. 1, 1986, p. 105-109.

Research output: Contribution to journalArticle

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abstract = "Conventional plasma isoenzyme and enzyme values usually are normal during the first few hours of acute myocardial infarction. Thus definitive diagnosis may be delayed. We have shown recently that infarction in dogs can be detected within 1 hr after coronary occlusion by analysis of relative activities of MM creatine kinase (CK) isoforms in plasma. Isoforms of MM CK evolve through posttranslational modifications in plasma of the form released from tissue (MM(A)) to MM(B) and MM(C). In this study we quantified changes in isoform profiles in the first available plasma samples from patients with evolving myocardial infarction, from patients with angina, and from normal subjects. In the 26 control subjects, the ratio of MM(A) to MM(C) was 1.09 ± 0.45 (SE) (range 0.31 to 3.1; upper limit of normal [defined as the mean plus 2 SD] 2.5). In the seven control patients with coronary artery disease, the ratio of MM(A) to MM(C) was 1.3 ± 0.3 with a range of 0.5 to 2.5. In contrast, among the 28 patients with acute myocardial infarction, the ratio of MM(A) to MM(C) in the first available plasma sample averaged 14.6 ± 4.5 (p < .01 compared with both control groups). First available samples were obtained 3.9 ± 0.4 hr after the onset of pain. In 24 of 28 patients (86{\%}) the ratio of MM(A) to MM(C) was greater than 2.5. Thus unequivocal changes in isoform profiles were evident in samples in which total and MB CK were within normal limits (79.7 ± 6.2 IU/liter for total CK and 4.4 ± 0.4 IU/liter for MB CK in patients with infarction compared with 90 ± 6.5 and 68 ± 11 IU/liter for total CK and 4.5 ± 0.4 and 4 ± 0.8 IU/liter for MB CK in normal control subjects and patients with angina, respectively). Accordingly, diagnostic changes in CK isoform profiles occur early after the onset of acute myocardial infarction.",
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N2 - Conventional plasma isoenzyme and enzyme values usually are normal during the first few hours of acute myocardial infarction. Thus definitive diagnosis may be delayed. We have shown recently that infarction in dogs can be detected within 1 hr after coronary occlusion by analysis of relative activities of MM creatine kinase (CK) isoforms in plasma. Isoforms of MM CK evolve through posttranslational modifications in plasma of the form released from tissue (MM(A)) to MM(B) and MM(C). In this study we quantified changes in isoform profiles in the first available plasma samples from patients with evolving myocardial infarction, from patients with angina, and from normal subjects. In the 26 control subjects, the ratio of MM(A) to MM(C) was 1.09 ± 0.45 (SE) (range 0.31 to 3.1; upper limit of normal [defined as the mean plus 2 SD] 2.5). In the seven control patients with coronary artery disease, the ratio of MM(A) to MM(C) was 1.3 ± 0.3 with a range of 0.5 to 2.5. In contrast, among the 28 patients with acute myocardial infarction, the ratio of MM(A) to MM(C) in the first available plasma sample averaged 14.6 ± 4.5 (p < .01 compared with both control groups). First available samples were obtained 3.9 ± 0.4 hr after the onset of pain. In 24 of 28 patients (86%) the ratio of MM(A) to MM(C) was greater than 2.5. Thus unequivocal changes in isoform profiles were evident in samples in which total and MB CK were within normal limits (79.7 ± 6.2 IU/liter for total CK and 4.4 ± 0.4 IU/liter for MB CK in patients with infarction compared with 90 ± 6.5 and 68 ± 11 IU/liter for total CK and 4.5 ± 0.4 and 4 ± 0.8 IU/liter for MB CK in normal control subjects and patients with angina, respectively). Accordingly, diagnostic changes in CK isoform profiles occur early after the onset of acute myocardial infarction.

AB - Conventional plasma isoenzyme and enzyme values usually are normal during the first few hours of acute myocardial infarction. Thus definitive diagnosis may be delayed. We have shown recently that infarction in dogs can be detected within 1 hr after coronary occlusion by analysis of relative activities of MM creatine kinase (CK) isoforms in plasma. Isoforms of MM CK evolve through posttranslational modifications in plasma of the form released from tissue (MM(A)) to MM(B) and MM(C). In this study we quantified changes in isoform profiles in the first available plasma samples from patients with evolving myocardial infarction, from patients with angina, and from normal subjects. In the 26 control subjects, the ratio of MM(A) to MM(C) was 1.09 ± 0.45 (SE) (range 0.31 to 3.1; upper limit of normal [defined as the mean plus 2 SD] 2.5). In the seven control patients with coronary artery disease, the ratio of MM(A) to MM(C) was 1.3 ± 0.3 with a range of 0.5 to 2.5. In contrast, among the 28 patients with acute myocardial infarction, the ratio of MM(A) to MM(C) in the first available plasma sample averaged 14.6 ± 4.5 (p < .01 compared with both control groups). First available samples were obtained 3.9 ± 0.4 hr after the onset of pain. In 24 of 28 patients (86%) the ratio of MM(A) to MM(C) was greater than 2.5. Thus unequivocal changes in isoform profiles were evident in samples in which total and MB CK were within normal limits (79.7 ± 6.2 IU/liter for total CK and 4.4 ± 0.4 IU/liter for MB CK in patients with infarction compared with 90 ± 6.5 and 68 ± 11 IU/liter for total CK and 4.5 ± 0.4 and 4 ± 0.8 IU/liter for MB CK in normal control subjects and patients with angina, respectively). Accordingly, diagnostic changes in CK isoform profiles occur early after the onset of acute myocardial infarction.

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