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Arch Pathol Lab Med. 1998 Mar;122(3):245-51.

A strategy for the use of cardiac injury markers (troponin I and T, creatine kinase-MB mass and isoforms, and myoglobin) in the diagnosis of acute myocardial infarction.

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Department of Clinical Chemistry, University of California, Davis, Health System, USA.



To design a strategy for cardiac injury marker testing in the diagnosis of acute myocardial infarction.


Prospective study. Group I (n=54 patients): evaluation of clinical performance. Specimens collected at 0, 3, 6, and 12 (+/-1.5) hours after presentation. World Health Organization criteria were used for diagnosis of acute myocardial infarction. Group II (n=57 patients): evaluation of temporal evolution. Time intervals 0 to 1.5, 1.5 to 4.5, 4.5 to 7.5, and 7.5 to 13.5 hours. Patients identified by positive creatine kinase-MB (CK-MB) mass or myoglobin. Fourteen patients in Group I qualified for Group II. Hence, the total number of patients was 97.


A team of laboratorians and clinicians at the University of California, Davis, hospital assessed the clinical performance and temporal evolution of serial CK-MB isoform, troponin I, and troponin T results in comparison to parallel CK-MB mass and myoglobin results.


Group I: sensitivity, specificity, and positive and negative predictive values. Group II: the time interval of the first positive result for each cardiac injury marker. Strategy and conclusions were based on study results and a literature review.


Emergency department patients with acute onset of chest pain and other complaints, possibly indicative of myocardial ischemia, who were under evaluation for admission.


Twenty-seven cases of acute myocardial infarction were documented. Group I: troponin I had the highest specificity (100%) and the highest positive predictive value (100%); troponin I, troponin T, and CK-MB mass had the highest sensitivity (90.0%); and the negative predictive values of troponin I, troponin T, and CK-MB mass were comparable (97.8%, 97.6%, and 97.6%, respectively). Group II: early diagnosis (within 1.5 hours) was provided by both CK-MB isoforms and CK-MB mass, and then by myoglobin and troponins, in order of decreasing frequency.


Creatine kinase-MB mass, myoglobin, and troponin I were selected as the cardiac injury markers of choice at our institution. The strategy calls for serial testing of myoglobin and CK-MB mass initially-and serially if warranted by heightened clinical suspicion--with troponin I added if indicated for (1) specific confirmation, (2) late presentation, or (3) risk stratification.

[Indexed for MEDLINE]

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