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M Müller-Bardorff

Publications and source records attributed to M Müller-Bardorff.

36 records · Page 2Linked to original sources
PubMed1998

Clinical performance of the new cardiac markers troponin T and CK-MB on the Elecsys 2010. A multicentre evaluation.

Elecsys assays for the cardiac markers Troponin T (cTnT) and CK-MB have been evaluated in an international multicenter study on the random access analyzer Elecsys 2010 to characterize their clinical performance and their comparability with respective established routine methods. In method comparison studies of Elecsys Troponin T (TnT) with Enzymun-Test TnT, good correlations (r > or = 0.95) and a high degree of correspondence (slopes in 4 laboratories between 0.95 and 1.05) were found. The method comparison studies of Elecsys CK-MB with various CK-MB routine methods lead to good correlations but some systematic deviation in the slopes due to varying standardization. In a reference population of 350 persons upper reference limits (97.5th percentile) of 0.03 milligrams/l for Elecsys TnT and 3.1 milligrams/l for Elecsys CK-MB were found. In cardiosensitivity studies the equivalent diagnostic information of the new Elecsys assays to routine methods was confirmed in the early diagnosis of acute myocardial infarction (AMI), the detection of minor myocardial damages in patients with unstable angina pectoris (UAP) and in time course data monitoring of AMI and bypass surgery patients. The superior sensitivity of cTnT versus CK-MB has been established in a screening situation where in 29 patients with cardiac diseases only cTnT, but not CK-MB, was found pathologically increased; this was due either to the larger diagnostic window of cTnT in AMI or to the more sensitive recognition of minor myocardial damage. In the same study, the cardiospecificity of Elecsys TnT was found to be at least 99.5%. This has also been demonstrated in an earlier study for Enzymun-Test TnT. Further cardiospecificity testing, e.g. in renal failure patients, showed results equivalent to those of Enzymun-Test TnT. An extended clinical study involving 294 patients with chest pain, of whom 58 had a final diagnosis of AMI, revealed highly comparable sensitivity and specificity for the Elecsys assays and routine methods. Thus, the already recommended clinical cut-off values of 0.1 milligrams/l for cTnT and 5 milligrams/l for CK-MB are also valid for the Elecsys assays. The slightly improved sensitivity of Elecsys TnT in the lower range even allows the recognition of pathological increase at cTnT concentrations below 0.1 milligrams/l in special situations with sufficient additional clinical information. Summarizing, provide the two cardiac markers on the Elecsys 2010 at least equivalent or even superior diagnostic information in various clinical situations of cardiac disease compared with routine methods. The short turn-around time and reliable performance qualify the Elecsys assays as new methods of choice for routine and emergency use.

Adult↗
PubMed1998

Biochemical markers in the diagnosis of coronary artery disease.

For many years cardiac markers have been used to classify whether chest pain is attributable to acute myocardial infarction or not. However massive, myocardial infarction is frequently preceded by plaque inflammation and local thrombus formation. Novel cardiac markers focus on detection of these more subtle manifestations of coronary artery disease. Detection of inflammation of coronary artery plaques is best achieved by measurement of C-reactive protein and fibrinogen, while thrombus formation may be assessed by testing for fibrin formation and platelet activation. When coronary flow is severely impaired minor myocardial injury will occur and cellular constituents may egress from damaged myocytes. Among the many cardiac markers for myocardial cell necrosis, troponin T revealed the highest sensitivity and cardio-specificity. The superior performance of troponin T has not only refined detection of myocardial cell necrosis but has also improved the risk stratification process and may even facilitate therapeutic decision making in patients with acute coronary syndrome. This review will summarize the characteristics and performance of diagnostic tools used for classification and risk stratification of patients with suspected myocardial injury.

Biomarkers↗
PubMed1997

An improved rapid troponin T test with a decreased detection limit: a multicentre study of the analytical and clinical performance in suspected myocardial damage.

In a multicentre study, we evaluated the analytical and diagnostic performance of the second version of the TROPT rapid test (TROPT 2, CARDIACT in the US). We tested TROPT 2 on 796 blood samples from 487 patients admitted on suspicion of myocardial infarction between 1 and 72 h after onset of symptoms and determined cTnT ELISA and CK MB mass in the corresponding serum samples. Frequency distributions of the results with TROPT 2 showed a detection limit of 0.18 microgram/l (for 50% positive results) as determined by the quantitative cTnT ELISA method. In a total of 796 samples the sensitivities in the detection of myocardial infarction (WHO criteria) 8-12 h after onset of symptoms were highest for cTnT ELISA (98%), followed by the rapid assay and CK MB mass (92%). A subgroup of 87 patients was primarily classified by the WHO criteria for definite infarction. Based on the maximum values within each patient time-series, diagnostic sensitivities for infarction were 100% for TROPT2, cTnT ELISA and CK MB mass. The corresponding specificities were 90%, 82% and 100%, respectively. After reclassification summarizing all cases of myocardial damage (acute and subacute myocardial infarctions and minor myocardial damage) the sensitivities were 87% (TROPT2), 100% (cTnT ELISA) and 71% (CK MB mass). The specificities of all three markers were 100%. Over 50% of all cases of minor myocardial damage were detected by TROPT 2. The clinical evaluation showed that the diagnostic performance of TROPT 2 is only slightly lower than that of cTnT ELISA.

Angina, Unstable↗
PubMed1997

Improved troponin T ELISA specific for cardiac troponin T isoform: assay development and analytical and clinical validation.

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 micrograms/L) or in test samples from 43 marathon runners and 24 patients with rhabdomyolysis and highly increased creatine kinase. TnT 2 was increased > 0.2 microgram/L in 5 of 40 patients with renal failure and in 4 of 20 muscular dystrophy patients. The detection limit is 0.012 microgram/L. Day-to-day imprecision (CV) within the range 0.19-14.89 micrograms/L was < 5.8%. In 4955 patients without myocardial damage, 99.6% had TnT < 0.10 microgram/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 micrograms/L, and 0.81 microgram/L, respectively.

Animals↗
PubMed1997

Multicenter evaluation of a second-generation assay for cardiac troponin T.

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 microg/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.

Artifacts↗
PubMed1996

Troponin T: a diagnostic marker for myocardial infarction and minor cardiac cell damage.

The diagnosis of acute myocardial infarction is straightforward when anginal pain is accompanied by typical ECG changes and in these patients measurements of cardiac markers are unnecessary in deciding whether thrombolytic therapy is appropriate. Cardiac markers in patients with acute ischaemic coronary syndromes, however, may serve to identify a high risk subgroup of patients with small acute infarctions or minor myocardial damage. In many patients with chest pain a valid diagnosis of myocardial cell injury depends on the result of biochemical assays. In 30% of patients with unstable angina, troponin T is elevated although myocardial infarction was ruled out by cardiac enzymes and ECG recordings. The outcome of these patients at 4 weeks and 6 months follow-up is not different from that of patients with definite myocardial infarction. To guide therapeutic decisions on these patients a troponin T test result needs to be available rapidly. The rapid troponin T test strip assay, which allows the determination of troponin T levels in whole blood at the patient's bedside, can be performed conveniently in the emergency room or in laboratories with less sophisticated equipment and has the potential to aid in the triage of chest pain patients and the selection of therapeutic strategies.

Angina, Unstable↗
PubMed1996

Multicentre evaluation of an immunological rapid test for the detection of troponin T in whole blood samples.

In a multicentre study we assessed the analytical and diagnostic performance of a rapid test (TROPT rapid test, Boehringer Mannheim; in the USA: CARDIACT) for cardiac troponin T compared to quantitative troponin T ELISA and creatine kinase-MB mass determinations. The rapid test requires 150 microliters of heparinized or EDTA whole blood; serum is not suitable. Interference testing with biotin, haemoglobin and 27 standard drugs yielded no significant influence in the physiological range. Skeletal muscle troponin T concentrations > or = 40 micrograms/l gave positive results with the rapid test. We used the rapid test for 369 samples from 203 patients with suspected acute coronary syndromes and compared the results to troponin T ELISA and creatine kinase-MB mass. 90 patients (44%) were primarily classified as having myocardial infarction by the WHO criteria. Twenty-two (20%) of the 113 non-myocardial infarction patients were unstable angina pectoris cases showing increased troponin T ELISA but not increased creatine kinase-MB mass values. Consequently, these were classified as minor myocardial damage cases. The rapid test was positive in 99% of all samples with a troponin T ELISA value > or = 0.30 micrograms/l and negative in 95 to 96% of all samples below this value. Diagnostic sensitivities for the detection of acute myocardial infarction within the first 12 hours after onset of pain were the same, 90%, for the rapid test, troponin T ELISA and creatine kinase-MB mass. After 48 hours, diagnostic sensitivity of creatine kinase-MB mass sharply decreased whereas that of the troponin T assays remained close to 100% beyond 72 hours after onset of symptoms. Diagnostic specificities for acute myocardial infarction (WHO) of all markers remained between 80 and 100% over this time. The diagnostic sensitivity of the rapid test for the detection of high risk unstable angina pectoris patients with minor myocardial damage was nearly the same as for troponin T ELISA. A major advantage of the rapid test is the ease of use and 20 minute turn around time. This facilitates the detection of increased troponin T at alternate sites.

Biomarkers↗
PubMed1995

Development and characterization of a rapid assay for bedside determinations of cardiac troponin T.

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 microL) 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 microgram/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.

Angina, Unstable↗
PubMed1994

[Modification of re-stenosis with drugs].

In the treatment of patients with symptomatic coronary artery disease using PTCA, success is limited due to restenosis rates ranging from 30-50% of the lesions treated. Medical approaches to reduce the rate of restenosis were therefore tested in a number of trials. However, in only a few randomized and controlled trials were positive effects reported. Inhibiting platelet aggregation through the use of anti-glycoprotein IIb/IIIa monoclonal antibody 7E3 and, in some studies, with 3 omega fatty acids, a significant reduction in the rate of restenosis was observed. Many trials testing less potent inhibitors of platelet aggregation, such as acetylsalicylic acid, prostacyclin, thromboxane A2 receptor antagonists, and ticlopidine as well as anticoagulants such as heparin or coumarin, calcium antagonists, ACE-inhibitors, antiproliferative agents such as colchicine, methylprednisolone, and angiopeptin were inconclusive or without a positive treatment effect. The results of a hirudin multicenter trial on the rate of restenosis (Helvetica Trial) will soon be reported. There are many possible reasons for these disappointing results, such as poor standardization of the invasive studies, in analyzing the degree of coronary artery stenoses, the inadequate sample size in many trials, and insufficient local drug concentrations as well as the lack of beneficial effects of the study medication. Thus, at present there is no effective treatment to reduce the restenosis rate following PTCA. However, it can be expected that potent antithrombins, or inhibitors of platelet aggregation, may be useful.

Angioplasty, Balloon, Coronary↗
PubMed1994

[Monitoring ischemia with new markers].

The measurement of cardiac enzymes is critical for the diagnosis of acute myocardial infarction. Cardiac enzymes, however, are by no means ideal marker molecules, primarily due to their non-specific tissue distribution and low concentration in cardiomyocytes. Many limitations of cardiac enzymes can be overcome by the measurement of cardiospecific troponin T or I with immunological techniques. In the evaluation of new diagnostic methods it is important to define the purpose of marker molecule measurement, i.e., monitoring of definite myocardial infarction or establishing the proper diagnosis in patients with suspected myocardial infarction. For monitoring of success of reperfusion therapy and for the detection of reocclusion short-lived perfusion markers with rapid appearance in circulation such as myoglobin, fatty acid binding protein or glycogenisophosphorylase BB are preferable. For proper diagnosis in patients with suspected acute myocardial infarction test systems with high sensitivity and specificity are needed due to the low prevalence of disease in the patients tested. Troponin T determinations are particularly useful in this group of patients. With troponin T determinations it could be shown that some patients so far classified as having unstable angina do in fact have microinfarction. These data indicate the need for re-definition of diagnostic criteria of acute myocardial infarction.

Biomarkers↗
PubMed1990

Measurement of free human leukocyte elastase and human leukocyte elastase/alpha 1 proteinase inhibitor complexes by an enzyme-linked immunosorbent assay.

We report on an ELISA procedure for the quantitative analysis of total human leukocyte (PMN)-elastase, i.e., the simultaneous determination of (i) free (non-complexed) PMN-elastase and of (ii) PMN-elastase that is complexed to alpha 1 proteinase inhibitor. Simultaneous detection of both forms of PMN-elastase was achieved using a monoclonal antibody that recognizes a PMN-elastase-specific epitope present on both the uncomplexed and the complexed form of the enzyme. The test system described is reliable, easy to perform and permits the determination of total PMN-elastase in complex biological fluids such as plasma or seminal fluid. It is to be expected that this test system will be useful for investigations of human PMN-elastase in biological specimens obtained from both normal and pathological conditions.

Antibodies, Monoclonal↗