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  • 1
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    Development and Characterization of a Rapid Assay for Bedside Determinations of Cardiac Troponin T
    Ovid Technologies (Wolters Kluwer Health) ; 1995
    In:  Circulation Vol. 92, No. 10 ( 1995-11-15), p. 2869-2875
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 92, No. 10 ( 1995-11-15), p. 2869-2875
    Abstract: Background The appearance of cardiac proteins in blood is the most specific and sensitive indicator of acute myocardial cell necrosis. The measurement of cardiac markers, however, is time consuming and requires sophisticated equipment. To facilitate the biochemical detection for acute myocardial cell necrosis, a whole-blood rapid assay device for cardiac troponin T detection was developed that provides a test result within 20 minutes. Methods and Results Monoclonal antibody M7 is labeled with gold particles, and antibody 1B10 is labeled with biotin. Both antibodies, as well as buffer substances and detergents, are adsorbed onto paper fleeces mounted below an application well. Heparinized blood (160 μL) applied to this well solubilizes the dry chemistry reagents. Blood cells are separated from plasma via a glass-fiber fleece. The immunocomplexes formed are concentrated within the reading zone by binding of the biotin-labeled antibody with streptavidine immobilized to the test device. Troponin T bound to the test device serves as a control. The detection limit of this assay is 0.18 μg/L with a cross-reactivity with skeletal troponin T of 0.5%. In clinical analyses involving 25 healthy volunteers, 62 patients with chest pain but without myocardial ischemia, 35 patients with acute myocardial infarction, 24 patients with minor myocardial cell damage due to radiofrequency ablation, and 35 patients with unstable angina, the rapid assay was comparable to the troponin T enzyme immunoassay in regard to sensitivity and specificity. Conclusions This newly developed assay allows accurate, rapid, and convenient diagnosis of acute myocardial cell necrosis.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.92.10.2869
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 1995
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  • 2
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    Risk Stratification in Patients With Inferior Acute Myocardial Infarction Treated by Percutaneous Coronary Interventions : The Role of Admission Troponin T
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Circulation Vol. 102, No. 17 ( 2000-10-24), p. 2038-2044
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 102, No. 17 ( 2000-10-24), p. 2038-2044
    Abstract: Background —Cardiac troponin T (cTnT) elevations on admission indicate a high-risk subgroup of patients with ST-segment elevation acute myocardial infarction (AMI). This finding has been attributed to less effective reperfusion after thrombolytic therapy. The aim of this study was to determine the role of admission cTnT on the efficacy of percutaneous coronary interventions (PCIs) in inferior AMI. Methods and Results —One hundred fifty-nine consecutive patients with inferior ST-segment AMI were enrolled and followed up for a mean of 448 days. Patients were stratified by cTnT on admission. A cTnT ≥0.1 μg/L was found in 58% of patients. These patients had longer time intervals from onset of symptoms to therapy ( P 〈 0.001) and higher 30-day (10.8% versus 1.5%, P =0.027) and long-term (17.2% versus 4.5%, P =0.023) cardiac mortalities. Rates of the combined end point of death, nonfatal reinfarction, and need for repeated target vessel revascularization procedures were not different in cTnT groups (log rank, 0.69; P =0.41). PCI was attempted in 93.3% of cTnT-positive and 98.5% cTnT-negative patients ( P =0.24) but was less frequently successful in patients with cTnT ≥0.1 μg/L (77.9% versus 96.9%, P 〈 0.001). Coronary stenting reduced 30-day and long-term cardiac mortality, particularly among cTnT-positive patients. In a multivariate analysis, cTnT indicated an ≈5-fold-higher risk (adjusted OR, 4.6; 95% CI, 0.79 to 27.11; P =0.089) and was a strong albeit not independent risk predictor. Conclusions —In inferior AMI, a positive admission cTnT is associated with lower success rates of direct PCI and higher rates of cardiac events over the short and long term. These patients benefit from coronary stenting.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.102.17.2038
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
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  • 3
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    Cardiac Troponin T for Prediction of Short- and Long-Term Morbidity and Mortality after Elective Open Heart Surgery
    Oxford University Press (OUP) ; 2004
    In:  Clinical Chemistry Vol. 50, No. 9 ( 2004-09-01), p. 1560-1567
    Details
    In: Clinical Chemistry, Oxford University Press (OUP), Vol. 50, No. 9 ( 2004-09-01), p. 1560-1567
    Abstract: Background: Increased cardiac troponins in blood are observed after virtually every open heart surgery, indicating perioperative myocardial cell injury. We sought to determine the optimum time point for blood sampling and the respective cutoff value of cardiac troponin T (cTnT) for risk assessment in patients undergoing cardiac surgery. Methods: In a series of 204 patients undergoing scheduled open heart surgery, mainly for coronary artery bypass grafting (n = 132) or valve repair (n = 27), cTnT concentrations were measured before and 4 and 8 h after cross-clamping and then daily for 7 days. Individual risk was assessed by use of the Cleveland Clinic Foundation Risk score and intraoperative risk indicators such as duration of cardiopulmonary bypass, cross-clamping, and perioperative release of cardiac markers. Patients were followed for 28 months. Results: Cardiac mortality, all-cause mortality rates, and rates of nonfatal acute myocardial infarction (AMI) at 28 months were 6.9%, 8.8%, and 6.8%, respectively. cTnT was higher in patients with Q-wave AMI or postoperative heart failure requiring inotropic support, and in nonsurvivors. The ROC curve revealed a cTnT ≥0.46 μg/L at 48 h as the optimum discriminator for long-term cardiac mortality. Stepwise logistic regression identified higher Cleveland Clinic Risk Score [odds ratio (OR) = 2.6 per point], cross-clamp time & gt;65 min (OR = 6.6), and cTnT (OR = 4.9) as significant and independent predictors of long-term cardiac mortality. Conclusions: A single postoperative cTnT measurement can be used to estimate myocardial cell injury that impacts long-term survival after open heart surgery. It adds independently to established risk indicators.
    Type of Medium: Online Resource
    ISSN: 0009-9147 , 1530-8561
    URL: Article
    DOI: 10.1373/clinchem.2004.031468
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2004
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  • 4
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    Cardiac troponin T in patients with end-stage renal disease: absence of expression in truncal skeletal muscle
    Oxford University Press (OUP) ; 1998
    In:  Clinical Chemistry Vol. 44, No. 5 ( 1998-05-01), p. 930-938
    Details
    In: Clinical Chemistry, Oxford University Press (OUP), Vol. 44, No. 5 ( 1998-05-01), p. 930-938
    Abstract: In patients with end-stage renal disease (ESRD), the serum concentration of cardiac troponin T (cTnT) may be increased without cardiac ischemia. One reason for this unexplained increase could be the extracardiac expression of cTnT. However, truncal skeletal muscle biopsies of five patients with ESRD showed no evidence of the expression of either cTnT mRNA (reverse transcription-PCR) or protein (immunoblot, immunofluorescence). We also measured the serum concentration of cTnT in 97 patients with ESRD. The serum cTnT concentration determined in both first and second generation cTnT assays was significantly lower P & lt;0.01 in patients with a low cardiac risk than in patients with positive indicators of coronary artery disease. The correlation between cTnT and indicators of coronary artery disease is consistent with the hypothesis that cTnT in the serum of patients with ESRD originates from the heart.
    Type of Medium: Online Resource
    ISSN: 0009-9147 , 1530-8561
    URL: Article
    DOI: 10.1093/clinchem/44.5.930
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 1998
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  • 5
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    Release Kinetics of Cardiac Troponin T in Survivors of Confirmed Severe Pulmonary Embolism
    Oxford University Press (OUP) ; 2002
    In:  Clinical Chemistry Vol. 48, No. 4 ( 2002-04-01), p. 673-675
    Details
    In: Clinical Chemistry, Oxford University Press (OUP), Vol. 48, No. 4 ( 2002-04-01), p. 673-675
    Type of Medium: Online Resource
    ISSN: 0009-9147 , 1530-8561
    URL: Article
    DOI: 10.1093/clinchem/48.4.673
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2002
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  • 6
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    Independent Prognostic Value of Cardiac Troponin T in Patients With Confirmed Pulmonary Embolism
    Ovid Technologies (Wolters Kluwer Health) ; 2000
    In:  Circulation Vol. 102, No. 2 ( 2000-07-11), p. 211-217
    Details
    In: Circulation, Ovid Technologies (Wolters Kluwer Health), Vol. 102, No. 2 ( 2000-07-11), p. 211-217
    Abstract: Background —Cardiac troponin T (cTnT) is a sensitive and specific marker, allowing the detection of even minor myocardial cell injury. In patients with severe pulmonary embolism (PE), myocardial ischemia may lead to progressive right ventricular dysfunction. It was therefore the purpose of this study to test the presence of cTnT and its prognostic implications in patients with confirmed PE. Methods and Results —Fifty-six consecutive patients with confirmed PE were enrolled in this prospective study. PE was confirmed by pulmonary angiography, lung scan, or echocardiography and subsidiary analyses. Severity of PE was assessed by a clinical scoring system, and cTnT was measured within 12 hours after admission. cTnT was elevated (≥0.1 μg/L) in 18 (32%) patients with massive and moderate PE but not in patients with small PE. In-hospital death (odds ratio 29.6, 95% CI 3.3 to 265.3), prolonged hypotension and cardiogenic shock (odds ratio 11.4, 95% CI 2.1 to 63.4), and need for resuscitation (odds ratio 18.0, 95% CI 2.6 to 124.3) were more prevalent in patients with elevated cTnT. cTnT-positive patients more often needed inotropic support (odds ratio 37.6, 95% CI 5.8 to 245.6) and mechanical ventilation (odds ratio 78.8, 95% CI 9.5 to 653.2). After adjustment, cTnT remained an independent predictor of 30-day mortality (odds ratio 15.2, 95% CI 1.22 to 190.4). Conclusions —cTnT may improve risk stratification in patients with PE and may aid in the identification of patients in whom a more aggressive therapy may be warranted.
    Type of Medium: Online Resource
    ISSN: 0009-7322 , 1524-4539
    URL: Article
    DOI: 10.1161/01.CIR.102.2.211
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2000
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  • 7
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    Multicenter evaluation of a second-generation assay for cardiac troponin T
    Oxford University Press (OUP) ; 1997
    In:  Clinical Chemistry Vol. 43, No. 10 ( 1997-10-01), p. 1877-1884
    Details
    In: Clinical Chemistry, Oxford University Press (OUP), Vol. 43, No. 10 ( 1997-10-01), p. 1877-1884
    Abstract: We report on the evaluation of the second-generation assay for cardiac troponin T (cTnT) on the Enzymun®system. This new assay is completely specific for the cardiac isoform of TnT, utilizing two cardiospecific monoclonal antibodies. The assay time is reduced to 45 min. The interassay precision shows a median CV of 5.5%; 20% interassay CV was found between 0.05 and 0.1 μg/L. The cardiosensitivity of the second-generation cTnT assay in patients with ischemic myocardial injury appears equivalent when compared with the first-generation assay. We found no falsely positive results in patients with skeletal muscle damage including multitraumas, surgery patients, and marathon runners who showed highly increased values with the unspecific first-generation assay. In Duchenne disease cTnT was still increased, but to a much lower extent. cTnT remains increased in renal failure, but to a lesser degree than with the first-generation assay. The cause of this increase remains unclear. Although a cross-reactivity of skeletal muscle TnT in the second-generation assay could be excluded by our findings, minor myocardial damage or expression of the cardiac isoform of TnT in regenerating muscles cannot be ruled out in those cases with apparently falsely increased cTnT values. The second-generation cTnT assay is a step forward in the combination of cardiosensitivity and cardiospecificity in biochemical markers for diagnosis of heart disease.
    Type of Medium: Online Resource
    ISSN: 0009-9147 , 1530-8561
    URL: Article
    DOI: 10.1093/clinchem/43.10.1877
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 1997
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  • 8
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    Improved troponin T ELISA specific for cardiac troponin T isoform: assay development and analytical and clinical validation
    Oxford University Press (OUP) ; 1997
    In:  Clinical Chemistry Vol. 43, No. 3 ( 1997-03-01), p. 458-466
    Details
    In: Clinical Chemistry, Oxford University Press (OUP), Vol. 43, No. 3 ( 1997-03-01), p. 458-466
    Abstract: The first generation of troponin T ELISA (TnT 1) can yield false-positive results in patients with severe skeletal muscle injury. Therefore, a cardiac-specific second-generation troponin T ELISA (TnT 2) was developed, in which the cross-reactive antibody 1B10 has been replaced by a high-affinity cardiac-specific antibody M11.7. No cross-reactivity of TnT 2 was observed with purified skeletal muscle troponin T (1000 μg/L) or in test samples from 43 marathon runners and 24 patients with rhabdomyolysis and highly increased creatine kinase. TnT 2 was increased & gt;0.2 μg/L in 5 of 40 patients with renal failure and in 4 of 20 muscular dystrophy patients. The detection limit is 0.012 μg/L. Day-to-day imprecision (CV) within the range 0.19–14.89 μg/L was & lt;5.8%. In 4955 patients without myocardial damage, 99.6% had TnT & lt;0.10 μg/L. Assay comparison (TnT 1 vs TnT 2) over the whole concentration range (i.e., in 323 samples from AMI-suspected patients) showed a slope, intercept, and standard error of estimate (Sey) of 1.18, 0.01 μg/L, and 0.81 μg/L, respectively.
    Type of Medium: Online Resource
    ISSN: 0009-9147 , 1530-8561
    URL: Article
    DOI: 10.1093/clinchem/43.3.458
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 1997
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  • 9
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    Troponin T and I Assays Show Decreased Concentrations in Heparin Plasma Compared with Serum: Lower Recoveries in Early than in Late Phases of Myocardial Injury
    Oxford University Press (OUP) ; 2000
    In:  Clinical Chemistry Vol. 46, No. 6 ( 2000-06-01), p. 817-821
    Details
    In: Clinical Chemistry, Oxford University Press (OUP), Vol. 46, No. 6 ( 2000-06-01), p. 817-821
    Abstract: Background: Heparinized plasma samples allow more rapid analysis than serum samples, but preliminary studies showed lower cardiac troponin T (cTnT) results in plasma. We undertook a multicenter study to characterize this effect for cTnT and cardiac troponin I (cTnI). Methods: Blood samples were collected with and without heparin at five hospitals. cTnT was measured by a “third generation” assay (Elecsys®), and cTnI was measured by a commercial immunoassay (IMMULITE®). Results: Mean cTnT was 15% lower in heparin sampling tubes than in serum. Measured concentrations of cardiac troponins also decreased with increasing heparin concentrations added to sera. Heparin-induced losses were greater in early than in late phases after onset of chest pain. Addition of heparin (∼100 IU/mL) to serial samples from nine acute myocardial infarction patients produced mean cTnT losses of 33% at 1–12 h after onset of chest pain, 17% at 13–48 h, and 7% after 48 h. The changing heparin effects were seen for both cTnT and cTnI during time courses of individual patients with myocardial infarction. Conclusion: We suggest that binding of heparin to troponins decreases immunoreactivity, especially in early phases of myocardial injury. The resulting losses may depend on the antibodies used in each troponin assay.
    Type of Medium: Online Resource
    ISSN: 0009-9147 , 1530-8561
    URL: Article
    DOI: 10.1093/clinchem/46.6.817
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2000
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  • 10
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    Quantitative Bedside Assay for Cardiac Troponin T: A Complementary Method to Centralized Laboratory Testing
    Oxford University Press (OUP) ; 1999
    In:  Clinical Chemistry Vol. 45, No. 7 ( 1999-07-01), p. 1002-1008
    Details
    In: Clinical Chemistry, Oxford University Press (OUP), Vol. 45, No. 7 ( 1999-07-01), p. 1002-1008
    Abstract: Background: In the evaluation of chest pain patients, whole blood bedside assays of highly specific cardiac molecules may be an attractive alternative to centralized clinical chemistry testing. We now report on an optimized test strip device for cardiac troponin T (cTnT) that can be analyzed by a cardiac reader for quantitative assessment of the test result. Methods and Results: The cTnT test strip reader measures, via a CCD camera, the reflectance of the signal line. For quantitative analysis, a calibration curve was constructed from 1030 samples of 252 consecutive patients with acute coronary syndromes. In a method comparison of 140 samples, the quantitative results of the cTnT test strip reader correlated closely with the results of the cTnT ELISA (r = 0.98; y = 0.85x + 0.002). Within-run and day-to-day (n = 10) mean CVs were between 11% and 16%, respectively. The cross-reactivity with skeletal troponin T was & lt;0.02%. In patients with myocardial infarction, 45% and 91% of all samples were positive on admission and at 4–8 h after the onset of symptoms, respectively. ROC curve analysis demonstrated a comparable efficiency of the cTnT test strip reader and the laboratory-based cTnT ELISA in patients with suspected myocardial infarction. Conclusions: It is now possible to quantitatively determine cTnT at the patient’s bedside with a rapid and convenient test device. This will facilitate the diagnostic work up of patients with suspected myocardial cell necrosis.
    Type of Medium: Online Resource
    ISSN: 0009-9147 , 1530-8561
    URL: Article
    DOI: 10.1093/clinchem/45.7.1002
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 1999
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