scholarly journals High-sensitive cardiac troponin-I facilitates timely detection of subclinical anthracycline-mediated cardiac injury

Author(s):  
Melissa Jones ◽  
Peter O’Gorman ◽  
Catherine Kelly ◽  
Niall Mahon ◽  
Maria C Fitzgibbon

Background Anthracycline drugs are effective anticancer agents, but their optimal use is limited in many patients by the associated cardiotoxicity, even at designated safe doses. As conventionally sensitive cardiac troponin-I assays fail to reliably quantify concentrations of cardiac troponin-I below 30 ng/L, we investigated the potential role of high-sensitive cardiac troponin-I in the detection of subclinical cardiomyocyte injury in patients treated with anthracycline agents. Methods Serial high-sensitive cardiac troponin-I concentrations were assessed in 84 patients, receiving anthracycline-containing ( n = 38) and non-anthracycline-containing ( n = 46) regimens. Results were assessed for change from pretreatment levels and evaluated according to unisex and gender-specific 99th percentiles (25 ng/L and M: 34 ng/L, F: 16 ng/L, respectively). Results A significant increase in high-sensitive cardiac troponin-I was observed in the anthracycline cohort following five cycles of treatment, with the greatest change correlating to an absolute δ increase of 30.7 ng/L in the early-dose group (early-dose group: P < 0.0001, late-dose group: P < 0.01 and continuous-dose group: P < 0.0001). Doxorubicin dose did not correlate directly with high-sensitive cardiac troponin-I concentrations (Spearman r < −0.22). No significant changes in high-sensitive cardiac troponin-I were reported among the non-anthracycline cohort with all measurements below the 99th percentiles. Conclusions Treatment with anthracycline-based chemotherapeutic regimen demonstrated significant elevations of high-sensitive cardiac troponin-I, indicative of subclinical cardiomyocyte damage. This study demonstrates a role for high-sensitive cardiac troponin-I in evaluating those patients where cardiotoxicity is a concern and a potential future role as a biomarker in optimizing cardioprotective treatments in patients receiving anthracycline therapy.

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.


2020 ◽  
Vol 78 ◽  
pp. 42
Author(s):  
Sjur H. Tveit ◽  
Peder L. Myhre ◽  
Helge Røsjø ◽  
Torbjørn Omland

2010 ◽  
Vol 98 (3) ◽  
pp. 356a
Author(s):  
Genaro A. Ramirez-Correa ◽  
Sonia Cortassa ◽  
Brian Stanley ◽  
Wei Dong Gao ◽  
Anne M. Murphy

2004 ◽  
Vol 10 (4) ◽  
pp. S56
Author(s):  
Ryosuke Nishio ◽  
Akira Matsumori ◽  
Taku Okazaki ◽  
Yoshimasa Tanaka ◽  
Tamotsu Mitsuiye ◽  
...  

2003 ◽  
Vol 49 (7) ◽  
pp. 1095-1104 ◽  
Author(s):  
Susann Eriksson ◽  
Miia Junikka ◽  
Päivi Laitinen ◽  
Kirsi Majamaa-Voltti ◽  
Henrik Alfthan ◽  
...  

Abstract Background: Cardiac troponin I (cTnI) is a sensitive marker of cardiac injury, but cTnI assays, like other immunoassays, are susceptible to interferences. We evaluated the presence of interfering substances by measuring the recovery of cTnI added to samples from volunteers and from patients with acute coronary syndromes (ACS). Methods: We added a ternary complex of human cardiac troponin (30–500 μg/L) or cTnI from serum to samples from healthy volunteers and ACS patients. We measured cTnI with a two-site sandwich time-resolved immunofluorometric assay using two antibodies against epitopes in the central stable part of cTnI. We also analyzed 108 heparin-plasma samples from 16 ACS patients with this assay, with an assay based on four antibodies, and with two commercial cTnI assays, AxSYM and ACS:180. Results: In samples from both healthy persons and ACS patients, recoveries for our assay were 1–167% (range). Recoveries were increased by addition of an antibody with an epitope in the N-terminal region of cTnI to the solid phase and an antibody with an epitope in the C-terminal region as a second detection antibody. In 2 of 16 patients with ACS, normal cTnI concentrations found when measured with the original assay demonstrated clinically abnormal (up to 10-fold higher) results with the additional N- and C-terminal antibodies in the early phase of infarction. Both commercial cTnI assays also demonstrated clinically misleading, falsely low cTnI concentrations. Conclusions: Some yet unidentified, variable component, present in the blood from healthy volunteers and ACS patients, interferes with the binding of antibodies against epitopes in the central part of cTnI used in two commercial assays. Our approach to supplement the mid-fragment cTnI antibodies with antibodies in the N- and C-terminal parts of the molecule in an experimental assay represents a step in resolving this interferent.


2010 ◽  
Vol 38 (2) ◽  
pp. 287-291 ◽  
Author(s):  
Sally Brady ◽  
Malcolm York ◽  
Cheryl Scudamore ◽  
Thomas Williams ◽  
William Griffiths ◽  
...  

Circulation ◽  
1993 ◽  
Vol 88 (1) ◽  
pp. 101-106 ◽  
Author(s):  
J E Adams ◽  
G S Bodor ◽  
V G Dávila-Román ◽  
J A Delmez ◽  
F S Apple ◽  
...  

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