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Fred S Apple - One of the best experts on this subject based on the ideXlab platform.
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Cardiac Troponin testing in patients with covid 19 a strategy for testing and reporting results
Clinical Chemistry, 2021Co-Authors: Peter A Kavsak, Stephen W Smith, Ola Hammarsten, Andrew Worster, Fred S AppleAbstract:BACKGROUND The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that emerged late in 2019 causing COVID-19 (coronavirus disease-2019) may adversely affect the cardiovascular system. Publications from Asia, Europe, and North America have identified Cardiac Troponin as an important prognostic indicator for patients hospitalized with COVID-19. We recognized from publications within the first 6 months of the pandemic that there has been much uncertainty on the reporting, interpretation, and pathophysiology of an increased Cardiac Troponin concentration in this setting. CONTENT The purpose of this mini-review is: a) to review the pathophysiology of SARS-CoV-2 and the cardiovascular system, b) to overview the strengths and weaknesses of selected studies evaluating Cardiac Troponin in patients with COVID-19, and c) to recommend testing strategies in the acute period, in the convalescence period and in long-term care for patients who have become ill with COVID-19. SUMMARY This review provides important educational information and identifies gaps in understanding the role of Cardiac Troponin and COVID-19. Future, properly designed studies will hopefully provide the much-needed evidence on the path forward in testing Cardiac Troponin in patients with COVID-19.
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high sensitivity Cardiac Troponin assays and unstable angina
European heart journal. Acute cardiovascular care, 2018Co-Authors: Yader Sandoval, Fred S Apple, Stephen W SmithAbstract:The term unstable angina has been conventionally applied to patients with myocardial ischemia without myocardial necrosis. However, while the clinical context has remained constant over time, the biomarkers of myocardial injury and acute myocardial infarction have evolved. High-sensitivity Cardiac Troponin assays have several key analytical differences from prior Cardiac Troponin assay generations, which may alter the diagnosis and frequency of unstable angina, as well as affect our understanding of previously developed risk stratification strategies. This document reviews the current challenges in regards to unstable angina when using high-sensitivity Cardiac Troponin I and T assays.
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Cardiac Troponin assays guide to understanding analytical characteristics and their impact on clinical care
Clinical Chemistry, 2017Co-Authors: Fred S Apple, Yader Sandoval, Allan S Jaffe, Jordi OrdonezllanosAbstract:BACKGROUND: Cardiac Troponin I (cTnI) and Cardiac Troponin T (cTnT) determinations are fixtures in clinical practice and research. Cardiac Troponin testing has been the standard of practice for the diagnosis of acute myocardial infarction (AMI), early rule-out, risk stratification, and outcomes assessment in patients presenting with acute coronary syndrome (ACS) and non-ACS myocardial injury. We recognize from reading the literature over the past several years how poorly understood the analytical characteristics are for cTnI and cTnT assays by laboratorians, clinicians, and scientists who use these assays. CONTENT: The purposes of this mini-review are (a) to define limit of blank, limit of detection, limit of quantification, and imprecision, (b) overview the analytical characteristics of the existing Cardiac Troponin assays, (c) recommend approaches to define a healthy (normal) reference population for determining the 99th percentile and the appropriate statistic to use for this calculation, (d) clarify how an assay becomes designated as “high sensitivity,” and (e) provide guidance on determining delta (Δ) change values. SUMMARY: This review raises important educational information regarding cTnI and cTnT assays, their 99th percentile upper reference limits (URL) differentiated by sex, and specifically addresses high-sensitivity (hs)-assays used to measure low concentrations. Recommendations are made to help clarify the nomenclature and analytical and clinical characteristics to define hs-assays. The review also identifies challenges for the evolving implementation of hs-assays into clinical practice. It is hoped that with the introduction of these concepts, laboratorians, clinicians and researchers can develop a more unified view of how these assays should be used worldwide.
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the global need to define normality the 99th percentile value of Cardiac Troponin
Clinical Chemistry, 2014Co-Authors: Yader Sandoval, Fred S AppleAbstract:BACKGROUND: How to select a presumably normal population for the establishment of 99th percentile cutoffs for Cardiac Troponin assays has not been adequately addressed. Lack of attention to this question can result in misleading medical decision cutoffs. CONTENT: From our review of the peer-reviewed literature, including international recommendations, no uniform procedure is followed and no uniform guideline has been published by experts or regulatory agencies to guide researchers or manufacturers of Cardiac Troponin assays in their quest to define the health or “normality” of a reference population that is used to establish an accurate 99th percentile value. As we progress globally into the era of high-sensitivity Cardiac Troponin assays, we propose several suggested approaches to define presumably normal individuals by use of clinical and biomarker surrogates. SUMMARY: Our uniform approach to defining who is normal and who may not be normal will help to define diagnostic and risk outcomes assessments in the management of patients with suspected myocardial injury, both for use in current clinical practice and clinical research, as well as for the potential future use of Cardiac Troponin in primary prevention.
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effect of population selection on 99th percentile values for a high sensitivity Cardiac Troponin i and t assays
Clinical Biochemistry, 2013Co-Authors: Gus Koerbin, Fred S Apple, Allan S Jaffe, Walter P Abhayaratna, Julia M Potter, Tricia Ravalico, Peter E HickmanAbstract:Abstract Objective Using objective laboratory and clinical criteria to more accurately determine the 99th percentile values for Cardiac Troponin I and T. Design and methods We measured Cardiac Troponin T and Cardiac Troponin I with high-sensitivity assays in a large cohort of apparently healthy community subjects and calculated 99th percentiles for different sexes and ages. Subjects with possible subclinical disease were eliminated based on objective laboratory criteria, eGFR and NT-proBNP, and clinical criteria, history and examination and echocardiogram. Results For men and women of all ages, separately, more than 50% of subjects were excluded using these criteria, with a lesser proportion of younger subjects being excluded. In men aged Conclusions For establishing Cardiac Troponin 99th percentiles, simply using self-reporting of health is insufficient. Objective laboratory measures and clinical and echocardiographic assessments are essential to define a healthy population, especially in older persons.
Allan S Jaffe - One of the best experts on this subject based on the ideXlab platform.
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high sensitivity Cardiac Troponin after Cardiac stress test a systematic review and meta analysis
Journal of the American Heart Association, 2019Co-Authors: Eslam Samaha, Allan S Jaffe, Audrey Avila, Mohammad A Helwani, Arbi Ben Abdallah, Mitchell G Scott, Peter NageleAbstract:Background The recent introduction of high‐sensitivity Cardiac Troponin (hs‐cTn) assays has allowed clinicians to measure hs‐cTn before and after Cardiac stress testing, but the hs‐cTn release patt...
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how is Cardiac Troponin released from injured myocardium
European heart journal. Acute cardiovascular care, 2018Co-Authors: Johannes Mair, Ola Hammarsten, Bertil Lindahl, Christian Muller, Evangelos Giannitsis, Kurt Huber, Martin Mockel, Mario Plebani, Kristian Thygesen, Allan S JaffeAbstract:Cardiac Troponin I and Cardiac Troponin T are nowadays the criterion biomarkers for the laboratory diagnosis of acute myocardial infarction due to their very high sensitivities and specificities for myocardial injury. However, still many aspects of their degradation, tissue release and elimination from the human circulation are incompletely understood. Myocardial injury may be caused by a variety of different mechanisms, for example, myocardial ischaemia, inflammatory and immunological processes, trauma, drugs and toxins, and myocardial necrosis is preceded by a substantial reversible prelethal phase. Recent experimental data in a pig model of myocardial ischaemia demonstrated Cardiac Troponin release into the circulation from apoptotic cardiomyocytes as an alternative explanation for clinical situations with increased Cardiac Troponin without any other evidence for myocardial necrosis. However, the comparably lower sensitivities of all currently available imaging modalities, including Cardiac magnetic resonance imaging for the detection of particularly non-focal myocardial necrosis in patients, has to be considered for Cardiac Troponin test result interpretation in clinical settings without any other evidence for myocardial necrosis apart from increased Cardiac Troponin concentrations as well.
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what to do when you question Cardiac Troponin values
European heart journal. Acute cardiovascular care, 2018Co-Authors: Johannes Mair, Bertil Lindahl, Christian Muller, Evangelos Giannitsis, Kurt Huber, Martin Mockel, Mario Plebani, Kristian Thygesen, Allan S JaffeAbstract:High-sensitivity Cardiac Troponin assays enable Cardiac Troponin measurement with a high degree of analytical sensitivity and a low level of analytical imprecision at the low measuring range. One of the most important advantages of these new assays is that they allow novel, more rapid approaches for ruling in or ruling out acute myocardial infarctions. The increase in the early diagnostic sensitivity of high-sensitivity Cardiac Troponin assays comes at the cost of a reduced acute myocardial infarction specificity of the biomarker, because more patients with other causes of acute or chronic myocardial injury without overt myocardial ischaemia are detected than with previous Cardiac Troponin assays. Increased Troponin concentrations that do not fit with the clinical presentation are seen in the daily routine, mainly as a result of a variety of pathologies, and if tested in the same sample, even discrepancies between high-sensitivity Cardiac Troponin I and Troponin T test results may sometimes be found as well. In addition, analytically false-positive test results occasionally may occur since no assay is perfect. In this review, we summarise the biochemical, pathophysiological and analytical background of the work-up for such a clinical setting.
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abstract 20591 high sensitivity Cardiac Troponin after Cardiac stress test a meta analysis
Circulation, 2017Co-Authors: Eslam Samaha, Allan S Jaffe, Audrey Avila, Mohammad A Helwani, Arbi Ben Abdallah, Mitchell G Scott, Peter NageleAbstract:Introduction: Rising patterns of high-sensitivity Cardiac Troponin (hscTn) do not only occur during acute coronary syndrome, but also following cardiovascular stress. To improve our understanding a...
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Cardiac Troponin assays guide to understanding analytical characteristics and their impact on clinical care
Clinical Chemistry, 2017Co-Authors: Fred S Apple, Yader Sandoval, Allan S Jaffe, Jordi OrdonezllanosAbstract:BACKGROUND: Cardiac Troponin I (cTnI) and Cardiac Troponin T (cTnT) determinations are fixtures in clinical practice and research. Cardiac Troponin testing has been the standard of practice for the diagnosis of acute myocardial infarction (AMI), early rule-out, risk stratification, and outcomes assessment in patients presenting with acute coronary syndrome (ACS) and non-ACS myocardial injury. We recognize from reading the literature over the past several years how poorly understood the analytical characteristics are for cTnI and cTnT assays by laboratorians, clinicians, and scientists who use these assays. CONTENT: The purposes of this mini-review are (a) to define limit of blank, limit of detection, limit of quantification, and imprecision, (b) overview the analytical characteristics of the existing Cardiac Troponin assays, (c) recommend approaches to define a healthy (normal) reference population for determining the 99th percentile and the appropriate statistic to use for this calculation, (d) clarify how an assay becomes designated as “high sensitivity,” and (e) provide guidance on determining delta (Δ) change values. SUMMARY: This review raises important educational information regarding cTnI and cTnT assays, their 99th percentile upper reference limits (URL) differentiated by sex, and specifically addresses high-sensitivity (hs)-assays used to measure low concentrations. Recommendations are made to help clarify the nomenclature and analytical and clinical characteristics to define hs-assays. The review also identifies challenges for the evolving implementation of hs-assays into clinical practice. It is hoped that with the introduction of these concepts, laboratorians, clinicians and researchers can develop a more unified view of how these assays should be used worldwide.
Bertil Lindahl - One of the best experts on this subject based on the ideXlab platform.
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how is Cardiac Troponin released from injured myocardium
European heart journal. Acute cardiovascular care, 2018Co-Authors: Johannes Mair, Ola Hammarsten, Bertil Lindahl, Christian Muller, Evangelos Giannitsis, Kurt Huber, Martin Mockel, Mario Plebani, Kristian Thygesen, Allan S JaffeAbstract:Cardiac Troponin I and Cardiac Troponin T are nowadays the criterion biomarkers for the laboratory diagnosis of acute myocardial infarction due to their very high sensitivities and specificities for myocardial injury. However, still many aspects of their degradation, tissue release and elimination from the human circulation are incompletely understood. Myocardial injury may be caused by a variety of different mechanisms, for example, myocardial ischaemia, inflammatory and immunological processes, trauma, drugs and toxins, and myocardial necrosis is preceded by a substantial reversible prelethal phase. Recent experimental data in a pig model of myocardial ischaemia demonstrated Cardiac Troponin release into the circulation from apoptotic cardiomyocytes as an alternative explanation for clinical situations with increased Cardiac Troponin without any other evidence for myocardial necrosis. However, the comparably lower sensitivities of all currently available imaging modalities, including Cardiac magnetic resonance imaging for the detection of particularly non-focal myocardial necrosis in patients, has to be considered for Cardiac Troponin test result interpretation in clinical settings without any other evidence for myocardial necrosis apart from increased Cardiac Troponin concentrations as well.
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what to do when you question Cardiac Troponin values
European heart journal. Acute cardiovascular care, 2018Co-Authors: Johannes Mair, Bertil Lindahl, Christian Muller, Evangelos Giannitsis, Kurt Huber, Martin Mockel, Mario Plebani, Kristian Thygesen, Allan S JaffeAbstract:High-sensitivity Cardiac Troponin assays enable Cardiac Troponin measurement with a high degree of analytical sensitivity and a low level of analytical imprecision at the low measuring range. One of the most important advantages of these new assays is that they allow novel, more rapid approaches for ruling in or ruling out acute myocardial infarctions. The increase in the early diagnostic sensitivity of high-sensitivity Cardiac Troponin assays comes at the cost of a reduced acute myocardial infarction specificity of the biomarker, because more patients with other causes of acute or chronic myocardial injury without overt myocardial ischaemia are detected than with previous Cardiac Troponin assays. Increased Troponin concentrations that do not fit with the clinical presentation are seen in the daily routine, mainly as a result of a variety of pathologies, and if tested in the same sample, even discrepancies between high-sensitivity Cardiac Troponin I and Troponin T test results may sometimes be found as well. In addition, analytically false-positive test results occasionally may occur since no assay is perfect. In this review, we summarise the biochemical, pathophysiological and analytical background of the work-up for such a clinical setting.
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application of Cardiac Troponin in cardiovascular diseases other than acute coronary syndrome
Clinical Chemistry, 2017Co-Authors: Kai M Eggers, Bertil LindahlAbstract:BACKGROUND: Increased Cardiac Troponin concentrations in acute coronary syndrome (ACS) identify patients with ongoing cardiomyocyte necrosis who are at increased risk. However, with the use of more precise assays, Cardiac Troponin increases are commonly noted in other cardiovascular conditions as well. This has generated interest in the use of Cardiac Troponin for prognostic assessment and clinical management of these patients. In this review, we have summarized the data from studies investigating the implications of Cardiac Troponin concentrations in various acute and chronic conditions beyond ACS, i.e., heart failure, myocarditis, Takotsubo cardiomyopathy, aortic dissection, supraventricular arrhythmias, valve disease, pulmonary arterial hypertension, stroke, and in the perioperative setting. CONTENT: Cardiac Troponin concentrations are often detectable and frankly increased in non-ACS conditions, in particular when measured with high-sensitivity (hs) assays. With the exception of myocarditis and Takotsubo cardiomyopathy, Cardiac Troponin concentrations carry strong prognostic information, mainly with respect to mortality, or incipient and/or worsening heart failure. Studies investigating the prognostic benefit associated with Cardiac Troponin–guided treatments however, are almost lacking and the potential role of Cardiac Troponin in the management of non-ACS conditions is not defined. SUMMARY: Increased Cardiac Troponin indicates increased risk for adverse outcome in patients with various cardiovascular conditions beyond ACS. Routine measurement of Cardiac Troponin concentrations can however, not be generally recommended unless there is a suspicion of ACS. Nonetheless, any finding of an increased Cardiac Troponin concentration in a patient without ACS should at least prompt the search for possible underlying conditions and these should be managed meticulously according to current guidelines to improve outcome.
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short and long term individual variation in Cardiac Troponin in patients with stable coronary artery disease
Clinical Chemistry, 2013Co-Authors: Anna M Nordenskjold, Allan S Jaffe, Kai M Eggers, Per Venge, Hakan Ahlstrom, Ole Frobert, Bertil LindahlAbstract:BACKGROUND: A rise or fall of Cardiac Troponin is a prerequisite for the diagnosis of acute myocardial infarction. Defining significant changes requires knowledge of both biological and analytical ...
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Cardiac Troponin a critical review of the case for point of care testing in the ed
American Journal of Emergency Medicine, 2012Co-Authors: Roland Bingisser, Johannes Mair, Bertil Lindahl, Mauro Panteghini, Charles B Cairns, Michael Christ, P Hausfater, Christopher P Price, Per VengeAbstract:The measurement of Cardiac Troponin concentrations in the blood is a key element in the evaluation of patients with suspected acute coronary syndromes, according to current guidelines, and contribu ...
Robert H Christenson - One of the best experts on this subject based on the ideXlab platform.
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high sensitive Cardiac Troponin t as an early biochemical signature for clinical and subclinical heart failure
Circulation, 2017Co-Authors: Stephen L Seliger, James A De Lemos, Robert H Christenson, Susie N Hong, Richard A Kronmal, Lori B Daniels, Joao A C Lima, Alain G Bertoni, Christopher R DefilippiAbstract:Background:Although small elevations of high-sensitive Cardiac Troponin T (hs-cTnT) are associated with incident heart failure (HF) in the general population, the underlying mechanisms are not well...
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analytical and assay issues for use of Cardiac Troponin testing for risk stratification in primary care
Clinical Biochemistry, 2013Co-Authors: Robert H ChristensonAbstract:Abstract Cardiac Troponin is the standard marker for diagnosis of acute myocardial infarction and risk stratification of patients who present to an emergency department with signs and symptoms of acute Cardiac ischemia. Over the past few years, the analytical sensitivity of assays for Cardiac Troponin has improved significantly to the point where a detectable amount of Troponin can be measured in essentially all healthy subjects. Recent studies have shown that use of a highly sensitive Troponin assays may provide value to traditional markers of primary disease risk for patients, i.e., for those who have no history of heart disease. There are barriers to the adoption of Cardiac Troponin for screening high risk cohorts such as the elderly, diabetics and perhaps even the asymptomatic population. Strategies used for the assignment of cutoff concentrations in acute care, i.e., the 99th percentile, may not be appropriate for primary care as changes over baseline levels may provide more accurate information of risk than cross-sectional results. A review of biological variation has shown that Cardiac Troponin as a biomarker has low index of individuality, indicating that reference values are of little utility. Whether or not Cardiac Troponin can be released in reversible injury is a debate that could have significance for detecting minor myocardial injury. A major hurdle for use of Troponin in primary care is the lack of assay standardization and nomenclature for the different generations of Troponin assays. Standardization requires knowledge of what is released after Cardiac injury and what the various Cardiac Troponin assays are measuring. Currently it is not clear if the Cardiac Troponin release after ischemic injury is identical to that in circulation of healthy individuals. This may affect the design of future assays and standardization approaches. There is potential that a marker of myocardial injury such as Troponin can add to the value of existing indicators and biomarkers of cardiovascular disease risk. Additional analytical and clinical validations are needed to fully elucidate Cardiac Troponin metabolism and resolve ongoing clinical and laboratory issues. While these issues are directed to the use of Troponin in primary care, most of these concepts are relevant to the use of Troponin in acute coronary syndromes as well.
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influence of population selection on the 99th percentile reference value for Cardiac Troponin assays
Clinical Chemistry, 2012Co-Authors: Paul O Collinson, Robert H Christenson, Fred S Apple, David Gaze, Yen Ming Heung, Frances BoaAbstract:OBJECTIVE: We sought to determine the effect of patient selection on the 99th reference percentile of 2 sensitive and 1 high-sensitivity (hs) Cardiac Troponin assays in a well-defined reference population. METHODS: Individuals >45 years old were randomly selected from 7 representative local community practices. Detailed information regarding the participants was collected via questionnaires. The healthy reference population was defined as individuals who had no history of vascular disease, hypertension, or heavy alcohol intake; were not receiving Cardiac medication; and had blood pressure 60 mL · min−1 · (1.73 m2)−1, and normal Cardiac function according to results of echocardiography. Samples were stored at −70 °C until analysis for Cardiac Troponin I (cTnI) and Cardiac Troponin T (cTnT) and N-terminal pro-B–type natriuretic peptide. RESULTS: Application of progressively more stringent population selection strategies to the initial baseline population of 545 participants until the only individuals who remained were completely healthy according to the study criteria reduced the number of outliers seen and led to a progressive decrease in the 99th-percentile value obtained for the Roche hs-cTnT assay and the sensitive Beckman cTnI assay but not for the sensitive Siemens Ultra cTnI assay. Furthermore, a sex difference found in the baseline population for the hs-cTnT ( P = 0.0018) and Beckman cTnI assays ( P < 0.0001) progressively decreased with more stringent population selection criteria. CONCLUSIONS: The reference population selection strategy significantly influenced the 99th percentile reference values determined for Troponin assays and the observed sex differences in Troponin concentrations.
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validation of the 99th percentile cutoff independent of assay imprecision cv for Cardiac Troponin monitoring for ruling out myocardial infarction
Clinical Chemistry, 2005Co-Authors: Robert H Christenson, Fred S Apple, Curtis A Parvin, Kenneth F Buechler, Allan S JaffeAbstract:By definition, the probability that a single measured Cardiac Troponin result exceeds the estimated 99th percentile is equal to 0.01 (1%) for a person randomly selected from the general (reference) population. This is irrespective of the imprecision profile of the analytical method as well as the lack of standardization of Cardiac Troponin assays (1)(2)(3)(4)(5)(6)(7). However, the probability that a measured result exceeds the 99th percentile limit for a specific person from the reference population will vary depending on that person’s true concentration and on the imprecision profile of the specific analytical method. Furthermore, the overall probability that at least one of multiple measured values (the second or third measured Cardiac Troponin concentration in a timed series of Cardiac Troponin orders) exceeds the 99th percentile also will vary depending on the imprecision of the analytical method. To investigate the influence of assay imprecision on the likelihood of misclassifying healthy individuals or patients without myocardial injury, we simulated the distribution of Cardiac Troponin I (cTnI) results in a general population and added random analytical error reflecting different assay imprecision profiles. One imprecision profile assumes a CV of 37.5% at a cTnI of 0.05 μg/L, decreasing to a CV of 25% at a cTnI of 0.07 μg/L, …
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evaluation of imprecision for Cardiac Troponin assays at low range concentrations
Clinical Chemistry, 2004Co-Authors: Mauro Panteghini, Robert H Christenson, Fred S Apple, Johannes Mair, Franca Pagani, Kiangteck J Yeo, Francesco Dati, Jan RavkildeAbstract:Background: The European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction (MI) has recommended that an increased Cardiac Troponin should be defined as a measurement above the 99th percentile value of the reference group. A total imprecision (CV) at the decision limit of ≤10% is recommended. However, peer-reviewed data on assay imprecision are lacking. The purpose of this study was to construct the clinically relevant imprecision profiles for each of the commercially available Cardiac Troponin assays. Pools of human sera containing Cardiac Troponin concentrations around the MI decision limit were assessed to identify the lowest concentration associated with a 10% CV. Methods: Eight serum pools targeting different concentrations of Cardiac Troponin (I and T) were prepared and stored at −70 °C until usage. The Cardiac Troponin measurement protocol consisted of two replicates per specimen per run, and one run per day for 20 days, using two reagent lots and three calibrations. Manufacturers of each Cardiac Troponin assay directly performed the measurements. Data analysis for each assay was centralized and performed according to the NCCLS EP5-A guideline. Results: The lowest concentrations (μg/L) providing a 10% CV were as follows: AxSYM, 1.22; ACS:180, 0.37; Centaur, 0.33; Immuno 1, 0.34; Access, 0.06; Vidas, 0.36; Liaison, 0.065; Dimension, 0.26; Opus, 0.90; Stratus CS, 0.10; Immulite, 0.32; Vitros ECi, 0.44; Elecsys, 0.04; AIA 21, 0.09. Conclusion: No Cardiac Troponin assay was able to achieve the 10% CV recommendation at the 99th percentile reference limit defined by the manufacturer.
Scott W Sharkey - One of the best experts on this subject based on the ideXlab platform.
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Cardiac Troponin i Cardiac Troponin t and creatine kinase mb in dialysis patients without ischemic heart disease evidence of Cardiac Troponin t expression in skeletal muscle
Clinical Chemistry, 1997Co-Authors: Mary Mclaurin, Fred S Apple, Ellen M Voss, Charles A Herzog, Scott W SharkeyAbstract:Serum Cardiac Troponin T (cTnT) concentrations are frequently increased in chronic dialysis patients as measured by the first-generation ELISA immunoassay, as is creatine kinase (CK) MB mass in the absence of acute ischemic heart disease. We designed this study to compare four serum markers of myocardial injury [CK-MB mass, first-generation ELISA cTnT, second-generation Enzymun cTnT, and Cardiac Troponin I (cTnI)] in dialysis patients without acute ischemic heart disease. We also evaluated skeletal muscle from dialysis patients as a potential source of serum cTnT. No patients in the clinical evaluation group (n = 24) studied by history and by physical examination, electrocardiography, and two-dimensional echocardiography had evidence of ischemic heart disease. Biochemical markers were measured in serial predialysis blood samples with specific monoclonal antibody-based immunoassays. For several patients at least one sample measured above the upper reference limit: CK-MB, 7 of 24 (30%); ELISA cTnT, 17 of 24 (71%); Enzymun cTnT, 3 of 18 (17%); and cTnI, 1 of 24 (4%). In a separate group of dialysis patients (n = 5), expression of cTnT, but not cTnI, was demonstrated by Western blot analysis in 4 of 5 skeletal muscle biopsies. Chronic dialysis patients without acute ischemic heart disease frequently had increased serum CK-MB and cTnT. The specificity of the second-generation cTnT (Enzymun) assay was improved over that of the first-generation (ELISA) assay; cTnI was the most specific of the currently available biochemical markers. cTnT, but not cTnI, was expressed in the skeletal muscle of dialysis patients.
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Cardiac Troponin i Cardiac Troponin t and creatine kinase mb in dialysis patients without ischemic heart disease evidence of Cardiac Troponin t expression in skeletal muscle
Clinical Chemistry, 1997Co-Authors: Mary Mclaurin, Fred S Apple, Ellen M Voss, Charles A Herzog, Scott W SharkeyAbstract:Serum Cardiac Troponin T (cTnT) concentrations are frequently increased in chronic dialysis patients as measured by the first-generation ELISA immunoassay, as is creatine kinase (CK) MB mass in the absence of acute ischemic heart disease. We designed this study to compare four serum markers of myocardial injury [CK-MB mass, first-generation ELISA cTnT, second-generation Enzymun cTnT, and Cardiac Troponin I (cTnI)] in dialysis patients without acute ischemic heart disease. We also evaluated skeletal muscle from dialysis patients as a potential source of serum cTnT. No patients in the clinical evaluation group (n = 24) studied by history and by physical examination, electrocardiography, and two-dimensional echocardiography had evidence of ischemic heart disease. Biochemical markers were measured in serial predialysis blood samples with specific monoclonal antibody-based immunoassays. For several patients at least one sample measured above the upper reference limit: CK-MB, 7 of 24 (30%); ELISA cTnT, 17 of 24 (71%); Enzymun cTnT, 3 of 18 (17%); and cTnI, 1 of 24 (4%). In a separate group of dialysis patients (n = 5), expression of cTnT, but not cTnI, was demonstrated by Western blot analysis in 4 of 5 skeletal muscle biopsies. Chronic dialysis patients without acute ischemic heart disease frequently had increased serum CK-MB and cTnT. The specificity of the second-generation cTnT (Enzymun) assay was improved over that of the first-generation (ELISA) assay; cTnI was the most specific of the currently available biochemical markers. cTnT, but not cTnI, was expressed in the skeletal muscle of dialysis patients.
