scholarly journals Corrigendum to: A Possible Mechanism behind Faster Clearance and Higher Peak Concentrations of Cardiac Troponin I Compared with Troponin T in Acute Myocardial Infarction

2020 ◽  
Vol 66 (12) ◽  
pp. 1573-1573
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Cardiac Troponin I

Early Diagnostic Efficiency of Cardiac Troponin I and Troponin T for Acute Myocardial Infarction

1997 ◽  
Vol 4 (1) ◽  
pp. 13-21 ◽  
Author(s):  
John F. Tucker ◽  
Richard A. Collins ◽  
Alfred J. Anderson ◽  
Jacqueline Hauser ◽  
John Kalas ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Cardiac Troponin I ◽  
Diagnostic Efficiency ◽  
Early Diagnostic

scholarly journals A Possible Mechanism behind Faster Clearance and Higher Peak Concentrations of Cardiac Troponin I Compared with Troponin T in Acute Myocardial Infarction

2020 ◽  
Vol 66 (2) ◽  
pp. 333-341 ◽  
Author(s):  
Karin Starnberg ◽  
Vincent Fridén ◽  
Aida Muslimovic ◽  
Sven-Erik Ricksten ◽  
Susanne Nyström ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Heart Failure ◽  
Acute Myocardial Infarction ◽  
Cardiac Troponin ◽  
Cardiac Tissue ◽  
Troponin I ◽  
Troponin T ◽  
Cardiac Troponin I ◽  
Human Cardiac Tissue

Abstract Background Although cardiac troponin I (cTnI) and troponin T (cTnT) form a complex in the human myocardium and bind to thin filaments in the sarcomere, cTnI often reaches higher concentrations and returns to normal concentrations faster than cTnT in patients with acute myocardial infarction (MI). Methods We compared the overall clearance of cTnT and cTnI in rats and in patients with heart failure and examined the release of cTnT and cTnI from damaged human cardiac tissue in vitro. Results Ground rat heart tissue was injected into the quadriceps muscle in rats to simulate myocardial damage with a defined onset. cTnT and cTnI peaked at the same time after injection. cTnI returned to baseline concentrations after 54 h, compared with 168 h for cTnT. There was no difference in the rate of clearance of solubilized cTnT or cTnI after intravenous or intramuscular injection. Renal clearance of cTnT and cTnI was similar in 7 heart failure patients. cTnI was degraded and released faster and reached higher concentrations than cTnT when human cardiac tissue was incubated in 37°C plasma. Conclusion Once cTnI and cTnT are released to the circulation, there seems to be no difference in clearance. However, cTnI is degraded and released faster than cTnT from necrotic cardiac tissue. Faster degradation and release may be the main reason why cTnI reaches higher peak concentrations and returns to normal concentrations faster in patients with MI.

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.

scholarly journals Characterization of cardiac troponin subunit release into serum after acute myocardial infarction and comparison of assays for troponin T and I

1998 ◽  
Vol 44 (6) ◽  
pp. 1198-1208 ◽  
Author(s):  
Alan H B Wu ◽  
Yue-Jin Feng ◽  
Robert Moore ◽  
Fred S Apple ◽  
Paul H McPherson ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Troponin T ◽  
Cross Reactivity ◽  
Binary Complex ◽  
Serum Samples ◽  
Binary And Ternary Complexes ◽  
The Cross

Abstract We examined the release of cardiac troponin T (cTnT) and I (cTnI) into the blood of patients after acute myocardial infarction (AMI). Three postAMI serum samples were applied in separate analytical runs onto a calibrated gel filtration column (Sephacryl S-200), and the proteins were separated by molecular weight. Using commercial cTnT and cTnI assays measured on collected fractions, we found that troponin was released into blood as a ternary complex of cTnT-I-C, a binary complex of cTnI-C, and free cTnT, with no free cTnI within the limits of the analytical methodologies. The serum samples were also examined after incubation with EDTA and heparin. EDTA broke up troponin complexes into individual subunits, whereas heparin had no effect on the assays tested. We added free cTnC subunits to 24 AMI serum samples and found no marked increase in the total cTnI concentrations, using an immunoassay that gave higher values for the cTnI-C complex than free cTnI. To characterize the cross-reactivity of cTnT and cTnI assays, purified troponin standards in nine different forms were prepared, added to serum and plasma pools, and tested in nine quantitative commercial and pre-market assays for cTnI and one approved assay for cTnT. All nine cTnI assays recognized each of the troponin I forms (complexed and free). In five of these assays, the relative responses for cTnI were nearly equimolar. For the remainder, the response was substantially greater for complexed cTnI than for free cTnI. Moreover, there was a substantial difference in the absolute concentration of results between cTnI assays. The commercial cTnT assay recognized binary and ternary complexes of troponin on a near equimolar basis. We conclude that all assays are useful for detection of cardiac injury. However, there are differences in absolute cTnI results due to a lack of mass standardization and heterogeneity in the cross-reactivities of antibodies to various troponin I forms.

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 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
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