Heterogeneity of serum creatine kinase isoenzyme-MM in acute myocardial infarction

1989 ◽  
Vol 10 (8-9) ◽  
pp. 579-583 ◽  
Author(s):  
John Williams ◽  
Katherine M. Williams ◽  
Thomas Märshall
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Creatine Kinase ◽  
Serum Creatine Kinase ◽  
Creatine Kinase Isoenzyme

heterogeneity of creatine kinase isoenzyme MM in serum in myocardial infarction: interconversion of the "normal" and "abnormal" sub-bands by glutathione

1990 ◽  
Vol 36 (5) ◽  
pp. 775-777 ◽  
Author(s):  
J Williams ◽  
K M Williams ◽  
T Marshall
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Creatine Kinase ◽  
Reduced Glutathione ◽  
Serum Creatine Kinase ◽  
Final Concentration ◽  
Oxidized Glutathione ◽  
Creatine Kinase Isoenzyme ◽  
Sequence Of Events ◽  
Opposite Sequence

Abstract We used isoelectric focusing (IEF) in polyacrylamide gels to investigate the effects of glutathione on the sub-bands of serum creatine kinase (CK; EC 2.7.3.2) isoenzyme MM in acute myocardial infarction. The intensity of the "abnormal" sub-bands c (pI 7.25), e (pI 6.85), and g (pI 6.50) increased, and that of the "normal" sub-bands 1 (pI 6.91), 2 (pI 6.65), and 3 (pI 6.35) decreased, following serum incubation with reduced glutathione (GSH, final concentration 1.25 mmol/L). Further incubation with oxidized glutathione (GSSG, final concentration 5 mmol/L) reversed this change and restored the original pattern, whereas GSSG at 7.5 mmol/L caused sub-bands c, e, and g to disappear and sub-bands 1, 2, and 3 to be enhanced. Sequential incubation of serum with 2.5 mmol of GSSG and 7.5 mmol of GSH per liter produced the opposite sequence of events; i.e., the "abnormal" sub-bands disappeared then reappeared (and GSH at 10 mmol/L enhanced their reappearance). At higher concentrations, glutathione (GSH or GSSG) impaired the detection of the CK-MM sub-bands after IEF, an effect that was "quenched" by heat-inactivated serum of low CK activity. Likewise, the intensity of tissue CK-MM (corresponding to myocardium extracted into 100 mmol/L Tris HCl buffer, pH 7.4) was greatly enhanced by adding heat-inactivated serum to the tissue extract before IEF. We discuss the significance of these findings for the diagnosis of myocardial infarction.

Heterogeneity of serum creatine kinase isoenzyme MM in myocardial infarction: clinical significance and post-synthetic conversion of "abnormal" sub-bands.

1989 ◽  
Vol 35 (2) ◽  
pp. 206-210 ◽  
Author(s):  
J Williams ◽  
K M Williams ◽  
T Marshall
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Creatine Kinase ◽  
Clinical Significance ◽  
Isoelectric Focusing ◽  
Normal Serum ◽  
Serum Creatine Kinase ◽  
Polyacrylamide Gels ◽  
Creatine Kinase Isoenzyme

Abstract We investigated the "abnormal" sub-bands of serum creatine kinase (CK; EC 2.7.3.2) isoenzyme MM in acute myocardial infarction (AMI), using isoelectric focusing in polyacrylamide gels, and compared the patterns with those for non-AMI patients and for athletes with increased CK. The "abnormal" sub-bands a (pI 7.55), b (pI 7.35), c (pI 7.25), d (pI 7.05), e (pI 6.85), f (pI 6.72), g (pI 6.50), h (pI 6.40), i (pI 6.28), j (pI 6.20), and k (pI 6.15), in common with "normal" sub-bands 1 (pI 6.91), 2 (pI 6.65), and 3 (pI 6.35), were less uniformly distributed in the AMI and demonstrated a faster rate of anodal conversion than in the non-AMI patients and athletes. "Abnormal" sub-bands a and b were detected only in the AMI patients. Incubation of myocardial CK-MM, predominantly CK-MM 1, with 2-mercaptoethanol, 15 mmol/L, resulted in conversion to the "abnormal" sub-bands b and c. Incubation of myocardial CK-MM with normal serum of low total CK yielded CK-MM 3, which on further incubation with 2-mercaptoethanol, 15 mmol/L, resulted in conversion to the "abnormal" sub-bands f and g. Comparable in vitro incubation of serum from AMI patients gave pattern changes consistent with conversion of CK-MM 1 to b, c; CK-MM 2 to d, e; and CK-MM 3 to f, g.

Clinical evaluation of an immunoinhibition procedure for creatine kinase-MB.

1980 ◽  
Vol 26 (1) ◽  
pp. 150-152
Author(s):  
D Obzansky ◽  
J A Lott
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Creatine Kinase ◽  
Sensitivity And Specificity ◽  
Clinical Evaluation ◽  
Creatine Kinase Isoenzyme ◽  
Creatine Kinase Mb ◽  
Diagnostic Sensitivity And Specificity ◽  
Creatine Kinase Isoenzyme Mb

Abstract We have clinically evaluated the Dade "Cardiozyme" immunoinhibition procedure for determination of creatine kinase isoenzyme MB (CK-MG) in 71 patients who were suspected of having had an acute myocardial infarction. Electrophoresis for CK-MB was also carried out. On the basis of diagnostic sensitivity and specificity for myocardial infarction, we found the Dade procedure for CK-MB to be somewhat inferior to electrophoresis. In 11 patients for whom the time of infarction was known, we observed normal CK-MB results for two of them by both immunoinhibition and electrophoresis during the first 24 h, but subsequently could detect abnormal CK-MB results by both methods. Thus in some patients such data are not helpful for making a diagnosis in the first 24 h. The Dade procedure is easy to perform, but lacks sensitivity in the region of low CK-MB activity, requires a very stable spectrophotometer, is imprecise, and produces negative numerical results in patients without myocardial infarction.

Diagnosis of acute myocardial infarction from two measurements of creatine kinase isoenzyme MB with use of nonparametric probability estimation.

1989 ◽  
Vol 35 (3) ◽  
pp. 444-447 ◽  
Author(s):  
L H Bernstein ◽  
I J Good ◽  
G I Holtzman ◽  
M L Deaton ◽  
J Babb
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Creatine Kinase ◽  
Bayes Factors ◽  
Probability Estimation ◽  
Posterior Odds ◽  
Creatine Kinase Isoenzyme ◽  
Time Of Admission ◽  
Bivariate Probability ◽  
Creatine Kinase Isoenzyme Mb

Abstract By using bivariate probability estimation for the diagnosis of acute myocardial infarction (AMI) we show how to overcome the difficulties encountered for patients whose clinical presentation is atypical and those encountered when multiple isoenzyme determinations are treated by univariate methods. We use the values for creatine kinase isoenzyme MB measured at the time of admission and 12 h later to estimate the Bayes factors in favor of AMI. The Bayes factors are compiled into a table that the clinician can use to estimate the posterior probability that a patient has AMI. The table of Bayes factors is based on data for a sample of 802 non-AMI patients and 180 AMI patients. Further to validate the method, we randomly chose 200 of the non-AMI and 50 of the AMI patients as an evaluation sample, then used the remaining 602 non-AMI and 130 AMI patients to recompute the Bayes factors. These Bayes factors were used to find the probability of AMI for each of the 250 patients in the evaluation sample. The method resulted in only one false positive and no false negatives. For the misclassified patient the measurements at admission and 12 h later were 1 and 11 U/L; the posterior odds were 15 to 1 in favor of AMI, but in fact the patient was non-AMI.

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