Evaluation of cardiac troponin I and T levels as markers of myocardial damage in doxorubicin-induced cardiomyopathy rats, and their relationship with echocardiographic and histological findings

Bertinchant, Jean-Pierre; Polge, Anne; Juan, Jean-Marie; Oliva-Lauraire, Marie-Claire; Giuliani, Isabelle; Marty-Double, C; Burdy, J.Y; Fabbro‐Peray, Pascale; Laprade, Michel; Balì, Jean-Pierre; Granier, Claude; Coussaye, J.-E. de La; Dauzat, M.

doi:10.1016/s0009-8981(03)00013-5

Cited by 99 publications

(71 citation statements)

References 37 publications

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“…Overall, identification of cardiac injury based on cTn increases was similar with both assays. This is in contrast to the findings of Bertinchant et al who suggested that cTnT was a better indicator of cardiac injury in rats treated with doxorubicin (Bertinchant et al 2003); our investigation, as well as those of Bertinchant, used a Beckman Access 1 and Elecsys STAT 1 Immunoassay to quantitate cTnI and cTnT concentrations, respectively. In the current study, the association between positive serum cTn responses with these assays (values above the assay LOD) and histological changes typical of doxorubicin-induced injury, including vacuolation of the atria and ventricles (Herman et al 1999), was greater at the higher doses and longer dosing FIGURE 2.-Serial measurements of cTnI using the Nanosphere highsensitivity assay and cardiac histopathology results in rats given a weekly combination of dexrazoxane (50 mg/kg) and doxorubicin (2 mg/kg).…”

Section: Discussioncontrasting

confidence: 90%

Comparison of Cardiac Troponin I and T, Including the Evaluation of an Ultrasensitive Assay, as Indicators of Doxorubicin-induced Cardiotoxicity

et al. 2013

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Cardiac troponin (cTn) has been utilized to assess acute myocardial injury, but the cTn response in active/ongoing chronic injury is not well documented. The purpose of this study was to characterize the cardiac troponin I (cTnI), cardiac troponin T (cTnT), high-sensitivity cTnI, hematology, and clinical chemistry responses in rats treated with doxorubicin. Rats treated with 1, 2, or 3 mg/kg/week (wk) of doxorubicin for 2, 4, or 6 wks were sacrificed after 0, 2, or 4 wks of recovery and compared to untreated controls and animals treated with doxorubicin/dexrazoxane (50 mg/kg/wk) or etoposide (1 and 3 mg/kg/wk). The incidence and mean magnitude of cTn response increased with increasing dose and/or duration of doxorubicin treatment. Conversely, dexrazoxane/doxorubicin was partially protective for cardiotoxicity, and minimal cardiotoxicity occurred with etoposide treatment. Both cTnI and cTnT effectively identified doxorubicin-induced injury as indicated by vacuolation of cardiomyocytes of the atria/ventricles. The association between the cTn responses and histological changes was greater at the higher total exposures, but the magnitude of cTn response did not match closely with histologic grade. The high-sensitivity cTnI assay was also effective in identifying cardiac injury. Alterations occurred in the hematology and clinical chemistry parameters and reflected both dose and duration of doxorubicin treatment.

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Section: Discussioncontrasting

confidence: 90%

Comparison of Cardiac Troponin I and T, Including the Evaluation of an Ultrasensitive Assay, as Indicators of Doxorubicin-induced Cardiotoxicity

et al. 2013

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“…Currently there is no optimal method that can be used for early detection of subclinical late cardiotoxicity. The role of biochemical cardiomarkers that reflect cardiomyocyte degeneration (serum levels of cTnT) and functional myocardial changes (serum levels of NT-proBNP) in early detection of cardiotoxicity of cytostatics have been evaluated in many clinical and experimental studies [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24][25].…”

Section: Discussionmentioning

confidence: 99%

“…Dose of CNS radiation (Gy) 18 (12)(13)(14)(15)(16)(17)(18)(19)(20)(21)(22)(23)(24) Values are presented as median (range). * patients previously treated with anthracyclines ‡ acute lymphoblastic leukemia § acute myeloblastic leukemia …”

Section: Cns Radiation 17mentioning

confidence: 99%

“…Biochemical cardiomarkers that reflect cardiomyocyte degeneration (serum levels of cardiac troponin T -cTnT) and functional myocardial changes (serum levels of N-terminal fragment of the brain natriuretic peptide precursor -NT-proBNP) of cancer patients treated with potentially cardiotoxic therapy have been evaluated in several clinical and experimental studies [8][9][10][11][12][13][14][15][16][17][18][19][20][21][22][23][24]. However only little information is available about the usefulness of biomarkers CTnT and NTproBNP in detection of late anthracycline cardiotoxicity (more than 5 years after diagnosis) in survivors of pediatric leukemia.…”

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confidence: 99%

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Long-term cardiac effects of treatment for childhood leukemia

Urbanová

Urbán²,

Šimková³

et al. 2010

neo

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Late cardiac complications in cancer survivors may develop from subclinical myocardial damage. Biochemical correlates of minimal myocardial changes can be analyzed using a commercially available rapid assay. Biomarkers are considered more sensitive markers of subclinical cardiotoxicity than conventional electrocardiographic and echocardiographic methods.The aim of this study was to determine the values of plasma N-terminal pro brain natriuretic peptide (NT-pro-BNP) and cardiac troponin T (cTnT) in asymptomatic childhood leukemia survivors after anthracycline therapy in comparison with healthy volunteers. The survivors also underwent a detailed echocardiography.Twenty six survivors of leukemia previously treated with anthracyclines with total cumulative dose 95-600 (median 221) mg/m 2 were evaluated. Analyses of cTnT and NT-proBNP from blood samples and echocardiography were performed 5-25 years after completion of therapy for childhood leukemia. Control group for biochemical analyses consisted of 22 age-and gender-matched apparently healthy volunteers.Values of NT-proBNP were significantly elevated in ANT group compared to controls (35.1 ± 37.8 vs. 9.6 ± 6.7 pg/ml, P<0.010). CTnT remained below the diagnostic cut-off values in both groups. All echocardiographic parameters of patients remained normal.In conclusion, differences in NT-proBNP values between patients treated with anthracyclines and healthy volunteers might signal an initial stage of anthracycline-induced myocardial damage. The potential of this biomarker to detect subclinical anthracycline-induced myocardial alterations before development of echocardiographic and clinical changes is promising. Key words: cardiotoxicity, natriuretic peptides, cardiac troponins, anthracyclines, echocardiographyNeoplasma 57, 2, 2010 doi:10.4149/neo_2010_02_179Abbreviations: ANT group -patients previously treated with anthracyclines; cTn -cardiac troponins; cTnT -cardiac troponinT; NPs -natriuretic peptides; NT-proBNP -N-terminal fragment of the brain natriuretic peptide precursor; LV -left ventricular; LVEDD -left ventricular end-diastolic diameter; LVESD -left ventricular end-systolic diameter; LA -left atrium dimension; RV -right ventricular dimension; EF -ejection fraction; E -early diastolic flow velocity; A -late diastolic flow velocity; DT -deceleration time; IVRT -left ventricular isovolumetric relaxation time; TDI -tissue Doppler imaging; Ea -early diastolic velocity of the medial mitral annulus; Em; Sa -systolic velocity; Am -late diastolic velocity

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“…Preus et al [9] reported the usefulness of LDH-1, LDH-2, and CK-MB, while various other authors reported troponin I and/or troponin T as markers for myocardial damage in rats [1,2,4,5,8,12]. Recently, the International Life Science Institute (ILSI) / Health Environmental Science Institute (HESI) have undertaken a comprehensive study focusing on the influence of methodological differences regarding troponin I detection in diluted samples of serum from rats treated with isoproterenol.…”

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confidence: 99%

Correlation among Clinicopathological Parameters of Myocardial Damage in Rats Treated with Isoproterenol

et al. 2007

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Abstract:The correlation among clinicopathological parameters of myocardial damage was investigated in rats administered a single subcutaneous dose of isoproterenol at 0 (saline), 0.04, 0.4 and 4 mg/kg. Total lactate dehydrogenase (LDH), creatine kinase (CK), and their isoenzymes (LDH-1, LDH-2 and CK-MB), as well as troponin I and tropinin T, were measured 4 h after the administration of the drug. Troponin I was determined by a chemiluminescence method using Bayer Centaur and DPC Immulyze, as well as by ELISA. Troponin T was assayed semi-quantitatively using Trop T Sensitive. A high correlation was found among LDH isoenzymes, troponin I (Centaur) and troponin T. The present result provides a baseline for interpreting changes in the different parameters of myocardial damage assayed by different methods in toxicity studies.

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Evaluation of cardiac troponin I and T levels as markers of myocardial damage in doxorubicin-induced cardiomyopathy rats, and their relationship with echocardiographic and histological findings

Cited by 99 publications

References 37 publications

Comparison of Cardiac Troponin I and T, Including the Evaluation of an Ultrasensitive Assay, as Indicators of Doxorubicin-induced Cardiotoxicity

Comparison of Cardiac Troponin I and T, Including the Evaluation of an Ultrasensitive Assay, as Indicators of Doxorubicin-induced Cardiotoxicity

Long-term cardiac effects of treatment for childhood leukemia

Correlation among Clinicopathological Parameters of Myocardial Damage in Rats Treated with Isoproterenol

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