Creatine kinase-MB, cardiac troponin T, and myoglobin levels identified failed reperfusion after thrombolysis in acute MI
ACP J Club. 1998 Nov-Dec; 129:71. doi:10.7326/ACPJC-1998-129-3-071
Stewart JT, French JK, Théroux P, et al. Early noninvasive identification of failed reperfusion after intravenous thrombolytic therapy in acute myocardial infarction. J Am Coll Cardiol. 1998 Jun;31:1499-505. [PubMed ID: 9626826]
Can creatine kinase-MB (CKMB), cardiac troponin T (troponin), and myoglobin levels identify failed reperfusion after intravenous thrombolytic therapy in acute myocardial infarction (MI)?
A blinded comparison of 3 biochemical markers and coronary arteriography.
Clinical centers in Canada and New Zealand.
105 patients (mean age 59 y, 78% men) who presented with typical ischemic chest pain > 20 minutes in duration and ≥ 1-mm ST-segment elevation in 2 contiguous electrocardiographic leads and who were treated with aspirin, 300 to 325 mg, and streptokinase, 1.5 million U by rapid infusion, plus heparin or hirulog.
Description of tests and diagnostic standard
Blood samples drawn before thrombolytic therapy and at 30, 60, 90, and 120 minutes were analyzed for levels of CKMB, troponin, and myoglobin. The diagnostic standard was a 90-minute arteriogram (Thrombolysis in Myocardial Infarction [TIMI] grade flow).
Main outcome measure
Sensitivity and specificity of biochemical marker ratios of failure to reperfuse (TIMI grade 0 to 2 flow in the infarction-related artery at 60 and 90 min).
The sensitivity, specificity, and likelihood ratios for biochemical marker ratios at 60 and 90 minutes are presented in the Table.
In patients with acute myocardial infarction, changes in the levels of creatine kinase-MB, cardiac troponin T, and myoglobin for periods of 60 and 90 minutes identified failed reperfusion.
Source of funding: In part, Health Research Council of New Zealand.
For correspondence: Dr. J.T. Stewart, Department of Cardiology, Green Lane Hospital, Green Lane West, Auckland 1003, New Zealand. FAX 64-9-631-0703.
Table. Test features of biochemical marker ratios for detecting failed reperfusion*
|60-minute marker (ratio†)||Sensitivity||Specificity||+LR||-LR|
|Creatine kinase-MB (1.5)||33%||85%||2.2||0.8|
|Creatine kinase-MB (5)||93%||60%||2.3||0.1|
|Cardiac troponin T (1.5)||70%||65%||2.0||0.5|
|Cardiac troponin T (5)||97%||43%||1.7||0.1|
|90-minute marker (ratio†)||Sensitivity||Specificity||+LR||-LR|
|Creatine kinase-MB (5)||82%||66%||2.4||0.3|
|Creatine kinase-MB (10)||91%||49%||1.8||0.2|
|Cardiac troponin T (5)||82%||67%||2.5||0.3|
|Cardiac troponin T (10)||95%||58%||2.3||0.1|
*Thrombolysis in Myocardial Infarction 0 to 2 grade flow. +LR = likelihood ratio for
presence of disease if the test is positive; -LR = likelihood ratio if the test is
negative. Both calculated from data in article.
†The ratio is the concentration of the marker protein after thrombolytic therapy was given divided by the pretreatment value.
The results of the study by Stewart and colleagues confirm previous findings showing that successful coronary reperfusion leads to an accelerated increase in the levels of plasma markers of myocardial injury in patients treated with thrombolytic therapy for MI (1-3). Changes in the level of myoglobin have been found in almost all previous studies to be useful in detecting coronary reperfusion but may lack specificity because this marker is not cardiac-specific. Rapid increases in CKMB, MB isoforms, and troponin may offer enhanced specificity but may be less sensitive because early changes in levels of these compounds are less marked than those of myoglobin. Differences also exist in the performance of the available assays for these markers. This is important for development of clinical criteria for failure of reperfusion. Nonetheless, available data suggest that using ratios of 60- and 90-minute levels to the initial levels of some of these markers is reasonably accurate for assessing the likelihood of coronary reperfusion, particularly when taken in the context of other such clinical variables as rapid resolution of ST-segment elevation. This and other studies also found that the rapid increases in these markers occur more frequently in patients with complete reperfusion (TIMI-3 flow) than in those with incomplete reperfusion (TIMI-2 flow).
Clinical use of these markers in noninvasive characterization of reperfusion depends on the availability of reliable quantitative assays that can be done within 30 minutes to permit additional intervention when indicated. Such rapid assays are unfortunately not widely available but should be soon.
Paul R. Eisenberg, MD, MPH
Washington UniversitySt. Louis, Missouri, USA
Paul R. Eisenberg, MD, MPH
St. Louis, Missouri, USA
1. Apple FS, Henry TD, Berger CR, Landt YA. Early monitoring of serum cardiac troponin I for assessment of coronary reperfusion following thrombolytic therapy. Am J Clin Pathol. 1996;105:6-10. [PubMed ID: 8561090]
2. Tanasijevic MJ, Cannon CP, Wybenga DR, et al. Myoglobin, creatine kinase MB, and cardiac troponin-I to assess reperfusion after thrombolysis for acute myocardial infarction: results from TIMI 10A. Am Heart J. 1997;134:622-30. [PubMed ID: 9351728]
3. Laperche T, Golmard JL, Steg PG. Early behavior of biochemical markers in patients with thrombolysis in myocardial infarction grade 2 flow in the infarct artery as opposed to other flow grades after intravenous thrombolysis for acute myocardial infarction. PERM Study Group. Prospective Evaluation of Reperfusion Markers.Am Heart J. 1997;134:1044-51. [PubMed ID: 9424064]