Prompt detection of myocardial injury by assay of creatine kinase isoforms in initial plasma samples

Abstract

Summary:To determine the sensitivity and specificity of assays of isoforms of the MM isoenzyme of creatine kinase (CK) and MB-CK for the diagnosis or exclusion of acute myocardial infarction in plasma samples obtained at the time of presentation to the emergency room of patients with suspected myocardial infarction, 50 patients in whom the diagnosis was ultimately established and 3 I in whom infarction was ultimately excluded were evaluated. Of the 50 patients in whom infarction was ultimately established, 47 had an increased ratio of the MM3 to the MMI isoform or elevated MB-CK in the plasma sample initially available. The specificity of the approach was 77%, sensitivity 94%. The availability of rapid assays for MM-CK isoforms and for MB-CK should facilitate determination of the presence or absence of acute myocardial injury sufficiently promptly so that decisions regarding treatment can be made optimally.

Biomarkers of Cardiac Injury: An Update

“…Criteria with MM isoforms have generally used an MM3-to-MM1 ratio above 0.5. 54 This is used in association with CKMB, since isoform ratios decline by the time CKMB elevations have occurred. However, they lack tissue specificity, similar to the problem with total CK.…”

Heterogeneity of mitochondrial creatine kinase

“…In the present study, the lysine residues in the C-terminus were removed by carboxypeptidase, and the pIs of delysined Mi-CKs changed to the more acidic side than those of the original Mi-CKs. The amino acid of the C-terminus of two cytosolic CKs (CK-M and CK-B) is also lysine, and is dissimilated by delysination with carboxypeptidase existing in serum at 267 ± 45 IU/l (mean ± standard deviation) in the intravascular circulation [31,32]. Therefore, the results suggest that Mi-CKs are dissimilated by carboxypeptidase in the intravascular circulation similar to cytosolic CKs.…”

Coronary Heart Disease Syndromes: Pathophysiology and Clinical Recognition

“…A previously preferred enzymatic technique was the measurement of CK and, in particular, the myocardium-specifi c CK-MB isoenzyme, measured by spectrophotometry, fl uorometry, or radioimmunoassay. [160][161][162][163][164][165][166][167][168][169][170][171][172][173][174][175] CK-MB usually increases in the sera of patients 2 to 3 hours after the onset of acute MI, reaches a peak at 10 to 12 hours, and returns to normal within 24 hours after the event in patients with small infarcts and in those who have reperfusion after endogenous thrombolysis. In patients with large infarcts, and those who fail to experience reperfusion, CK and CK-MB often peak later (e.g., 18 to 24 hours after infarction) and return to normal 30 to 40 hours after the event.…”

“…Measurements of CK isoforms, as well as myoglobin, have proved useful in detecting reperfusion after thrombolytic therapy or release of an experimental coronary artery occlusion. [169][170][171][172][173] The conversion of CK isoform from CKMM-1 to CKMM-2 in the peripheral circulation appears to correlate with successful reperfusion therapy. Staccato increases in serum myoglobin in the fi rst 4 to 6 hours after MI are indicative of reperfusion; rapid peaking of increases in serum CK and CK-MB (within 10 to 12 hours from symptom onset) are also often indicative of reperfusion of the MI.…”