Equivalent early sensitivities of myoglobin, creatine kinase MB mass, creatine kinase isoform ratios, and cardiac troponins I and T for acute myocardial infarction

1995 ◽  
Vol 41 (9) ◽  
pp. 1266-1272 ◽  
Author(s):  
J Mair ◽  
D Morandell ◽  
N Genser ◽  
P Lechleitner ◽  
F Dienstl ◽  
...  

Abstract Early sensitivities of creatine kinase (CK), CKMB (activity and mass), CKMM and CKMB isoform ratios, myoglobin, cardiac troponin I (cTnI), and cardiac troponin T (cTnT) were compared to find the most sensitive serum marker for acute myocardial infarction (AMI) during the first hours after onset of chest pain. In a prospective study we investigated 37 consecutive patients with AMI who were admitted to the coronary care unit within 4 h after onset of chest pain. Blood samples were drawn every hour for the first 10 h after admission. CKMB mass concentrations, CKMM and CKMB isoform ratios, myoglobin, cTnI, and cTnT increased significantly (P < or = 0.0067) earlier than CK and CKMB activity and were also significantly (P < or = 0.046) and markedly more sensitive on admission. Differences in early sensitivities of myoglobin, CKMB mass, CK isoform ratios, cTnI, and cTnT were small and not significant. Therefore, turnaround time and practicality for emergency determination of methods, specificities of markers, the required specificity in the individual patient, and costs mainly determine the choice among myoglobin, CKMB mass, CK isoforms, cTnI, and cTnT.

1994 ◽  
Vol 40 (7) ◽  
pp. 1291-1295 ◽  
Author(s):  
J E Adams ◽  
K B Schechtman ◽  
Y Landt ◽  
J H Ladenson ◽  
A S Jaffe

Abstract Although measurement of cardiac troponin I (cTnI) is, in some situations, more specific for detection of cardiac injury than is measurement of the MB isoenzyme of creatine kinase (MBCK), its sensitivity and specificity relative to MBCK for detection of myocardial infarction has not been established. Accordingly, we studied prospectively 199 consecutive patients admitted to the coronary care unit. Values of MBCK and cTnI mass were determined in all samples. Of the 188 patients admitted with a suspicion of acute myocardial ischemia, 89 were diagnosed as having an acute myocardial infarction on the basis of the patterns of MBCK values. Eighty-six of these patients also had increased cTnI (concordance, 96.6%); three did not. Of the patients diagnosed as without infarction, five with unstable angina and symptoms in the day(s) prior to admission had increased cTnI, for a cTnI specificity of 94.9%. Receiver operating characteristic curve analysis indicated that cTnI and MBCK had statistically indistinguishable diagnostic accuracies for the detection of acute myocardial infarction.


1997 ◽  
Vol 134 (4) ◽  
pp. 622-630 ◽  
Author(s):  
Milenko J. Tanasijevic ◽  
Christopher P. Cannon ◽  
Donald R. Wybenga ◽  
George A. Fischer ◽  
Christine Grudzien ◽  
...  

1997 ◽  
Vol 4 (1) ◽  
pp. 6-12 ◽  
Author(s):  
Gerard X. Brogan ◽  
Judd E. Hollander ◽  
Charles F. McCuskey ◽  
Henry C. Thode ◽  
Jeffrey Snow ◽  
...  

2011 ◽  
Vol 152 (38) ◽  
pp. 1528-1534 ◽  
Author(s):  
Eszter Szánthó ◽  
Zoltán Szabó ◽  
József Varga ◽  
György Paragh ◽  
Anna V. Oláh

Troponin is the first choice in the diagnosis of acute myocardial infarction. Correct interpretation is challenging, because high sensitive troponin tests used today detect even the smallest cardiac damage. Methods: High sensitive troponin T (Roche) and troponin I (Mitsubishi Pathfast) and creatine-kinase activity were measured in 20 patients, each having two samples with the time lapse 3–9 hours. Results: In the group without acute myocardial infarction (n = 10) no significant increase in creatine-kinase and creatine-kinase-MB levels were seen, and the mild raise of troponins was due to other cardiovascular problems (atrial fibrillation, paroxysmal supraventricular tachycardia). With acute myocardial infarction (n = 10) a dramatic increase of troponin levels was found in the second samples, and also an increase of creatine-kinase and creatine-kinase-MB activity. According to Fischer-probe a twofold or higher increase of troponin implies 19-times higher risk of acute myocardial infarction in the case of troponin T and 8-times odds ratio at troponin I. Conclusions: The patient’s accompanying diseases should always be considered. If the troponin level is elevated, the measurement should be repeated within 3–6 hours. When troponin shows at least a twofold increase and the patient has chest pain or positive ECG, AMI is likely, and the patient needs special medical care. Although the first troponin level might be elevated if accompanying diseases cause chronic cardiac damage, it can be differentiated by a second troponin measurement. Orv. Hetil., 2011, 152, 1528–1534.


2015 ◽  
Vol 156 (24) ◽  
pp. 964-971
Author(s):  
Ferenc Kovács ◽  
Ibolya Kocsis ◽  
Marina Varga ◽  
Enikő Sárváry ◽  
György Bicsák

Introduction: Cardiac biomarkers have a prominent role in the diagnosis of acute myocardial infarction. Aim: The aim of the authors was to study the diagnostic effectiveness of automated measurement of cardiac biomarkers. Method: Myeloperoxidase, high-sensitivity C-reactive protein, myoglobin, heart-type fatty acid binding protein, creatine kinase, creatine kinase MB, high-sensitivity troponin I and T were measured. Results: The high-sensitivity troponin I was the most effective (area under curve: 0.86; 95% confidence interval: 0.77–0.95; p<0.001) for the diagnosis of acute myocardial infarction. Considering a critical value of 0.35 ng/mL, its sensitivity and specificity were 81%, and 74%, respectively. Combined evaluation of the high-sensitivity troponin T and I, chest pain, and the electrocardiogram gave the best results for separation of acute myocardial infarction from other diseases (correct classification in 62.5% and 98.9% of patients, respectively). Conclusions: Until a more sensitive and specific cardiac biomarker becomes available, the best method for the diagnosis of acute myocardial infarction is to evaluate electrocardiogram and biomarker concentration and to repeat them after 3–6 hours. Orv. Hetil., 2015, 156(24), 964–971.


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