scholarly journals Evaluation of a New Assay for Cardiac Troponin I vs Creatine Kinase-MB for the Diagnosis of Acute Myocardial Infarction

1997 ◽  
Vol 4 (1) ◽  
pp. 6-12 ◽  
Author(s):  
Gerard X. Brogan ◽  
Judd E. Hollander ◽  
Charles F. McCuskey ◽  
Henry C. Thode ◽  
Jeffrey Snow ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Creatine Kinase ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
Creatine Kinase Mb

Comparable detection of acute myocardial infarction by creatine kinase MB isoenzyme and cardiac troponin I

1994 ◽  
Vol 40 (7) ◽  
pp. 1291-1295 ◽  
Author(s):  
J E Adams ◽  
K B Schechtman ◽  
Y Landt ◽  
J H Ladenson ◽  
A S Jaffe
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Creatine Kinase ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Characteristic Curve ◽  
Cardiac Injury ◽  
Cardiac Troponin I ◽  
Creatine Kinase Mb ◽  
Coronary Care

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.

Myoglobin, creatine kinase MB, and cardiac troponin-I to assess reperfusion after thrombolysis for acute myocardial infarction: Results from TIMI 10A

1997 ◽  
Vol 134 (4) ◽  
pp. 622-630 ◽  
Author(s):  
Milenko J. Tanasijevic ◽  
Christopher P. Cannon ◽  
Donald R. Wybenga ◽  
George A. Fischer ◽  
Christine Grudzien ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Creatine Kinase ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
Creatine Kinase Mb

scholarly journals Comparative analysis of cardiac troponin i and creatine kinase-MB as markers of acute myocardial infarction

1997 ◽  
Vol 20 (3) ◽  
pp. 269-271 ◽  
Author(s):  
Shazib Pervaiz ◽  
Dave Waskiewicz ◽  
F. Philip Anderson ◽  
Charlotte J. Lawson ◽  
Thomas P. Lohmann ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Creatine Kinase ◽  
Comparative Analysis ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
Creatine Kinase Mb

Simultaneous Rapid Measurement of Whole Blood Myoglobin, Creatine Kinase MB, and Cardiac Troponin I by the Triage Cardiac Panel for Detection of Myocardial Infarction

1999 ◽  
Vol 45 (2) ◽  
pp. 199-205 ◽  
Author(s):  
Fred S Apple ◽  
Robert H Christenson ◽  
Roland Valdes ◽  
Alexander J Andriak ◽  
Amy Berg ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Creatine Kinase ◽  
Whole Blood ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Point Of Care ◽  
Cardiac Troponin I ◽  
Clinical Sensitivity ◽  
Creatine Kinase Mb ◽  
Acute Mi

Abstract This multicenter study evaluated the Biosite Triage® Cardiac Panel as a quantitative, multimarker, whole blood system for the detection of acute myocardial infarction (MI). Optimum cutoffs for the discrimination of acute MI (n = 192 patients, 59 with MI) as determined by ROC curve analyses were as follows: 0.4 μg/L for cardiac troponin I (cTnI); 4.3 μg/L for the creatine kinase MB isoenzyme (CK-MB); and 107 μg/L for myoglobin. The Triage Panel showed the following concordances for detection or rule-out of MI compared with established devices: cTnI >89%; CK-MB >81%; myoglobin >69%. No significant differences were present between methods for the same marker. Diagnostic efficiencies demonstrated comparable sensitivities and specificities for the diagnosis of MI in patients presenting with symptoms compared with the Dade, Beckman, and Behring CK-MB, cTnI, and myoglobin assays; the ratio of sensitivity to specificity for each marker was as follows: cTnI, 98%:100%; CK-MB, 95%:91%; myoglobin, 81%:92%. The areas under the ROC curves for the Biosite myoglobin, CK-MB, and cTnI were 0.818, 0.905, and 0.970, respectively; the areas were significantly different, P <0.05. In patients with skeletal muscle injury and renal disease, the Triage cTnI showed 94% and 100% specificity, respectively. The Triage panel offers clinicians a whole blood, point-of-care analysis of multiple cardiac markers that provides excellent clinical sensitivity and specificity for the detection of acute MI.

scholarly journals Comparative sensitivity of cardiac troponin I and lactate dehydrogenase isoenzymes for diagnosing acute myocardial infarction

1996 ◽  
Vol 42 (11) ◽  
pp. 1770-1776 ◽  
Author(s):  
A S Jaffe ◽  
Y Landt ◽  
C A Parvin ◽  
D R Abendschein ◽  
E M Geltman ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Lactate Dehydrogenase ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Injury ◽  
Myocardial Damage ◽  
Cardiac Troponin I ◽  
Retrospective Diagnosis ◽  
Creatine Kinase Mb

Abstract Criteria for the retrospective diagnosis of acute myocardial infarction rely heavily on increases in lactate dehydrogenase (LD) isoenzymes. However, increases of LD isoenzyme activities are not specific for myocardial injury. Recently, increased concentrations of cardiac troponin I (cTnI) have been shown to be highly specific for myocardial damage and to have sensitivity comparable with that of creatine kinase MB isoenzyme for detecting cardiac injury. Furthermore, increases of cTnI persist in plasma for at least several days. The present study was designed to determine the relative sensitivities of cTnI and LD isoenzymes over time for the diagnosis of infarction. The results indicate that cTnI values are at least as sensitive as LD isoenzymes: 90% of patients with myocardial infarction had above-normal concentrations of cTnI on the 4th day after admission to the coronary care unit. Criteria based on cTnI should improve the accuracy of retrospective diagnoses of acute myocardial infarction.

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 ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Creatine Kinase ◽  
Chest Pain ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Turnaround Time ◽  
Serum Marker ◽  
Creatine Kinase Mb

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.

Abstract 2425: Absence of Auto-Antibodies against Cardiac Troponin I Predicts Improvement of Left Ventricular Function after Acute Myocardial Infarction

Circulation ◽  
2008 ◽  
Vol 118 (suppl_18) ◽  
Author(s):  
Florian Leuschner ◽  
Jin Li ◽  
Stefan Göser ◽  
Lars Reinhardt ◽  
Renate Öttl ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Stroke Volume ◽  
Antibody Titer ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Troponin I ◽  
Igg Antibody ◽  
Follow Up Study

Application of antibodies against cardiac troponin I (cTnI-Ab) can induce dilation and dysfunction of the heart in mice. Recently, we demonstrated that immunization with cTnI induces inflammation and fibrosis in myocardium of mice. Others have shown that autoanti-bodies to cTnI are present in patients with acute coronary syndrome. But little is known about the clinical relevance of detected cTnI-Ab. First, anti-cTnI and anti-cTnT antibody titers were measured in sera from 272 patients with dilated- (DCM) and 185 with ischemic- (ICM) cardiomyopathy. Secondly, 108 patients with acute myocardial infarction (AMI) were included for a follow-up study. Heart characteristics were determined by magnetic resonance imaging 4 days and 6 –9 months after AMI. Altogether, in 7,0% of patients with DCM and in 9,2% with ICM an anti-cTnI IgG antibody titer ≥1:160 was measured. In contrast, only in 1,7% of patients with DCM and in 0,5% with ICM an anti-cTnT IgG antibody titer ≥1:160 was detected. Ten out of 108 patients included in the follow-up study were tested positive for cTnI-Ab with IgG Ab titers ≥1:160. TnI-Ab negative patients showed a significant increase in LVEF and stroke volume 6 –9 months after AMI. In contrast, there was no significant increase in LVEF and stroke volume in TnI-Ab positive patients. We demonstrate for the first time that the prevalence of cTnI-Abs in patients with AMI has an impact on the improvement of the LVEF over a study period of 6 –9 months.

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