How Would the Reverend Bayes Interpret High-Sensitivity Troponin?
2010; Lippincott Williams & Wilkins; Volume: 121; Issue: 10 Linguagem: Inglês
10.1161/cir.0b013e3181d839e8
ISSN1524-4539
Autores Tópico(s)Coronary Interventions and Diagnostics
ResumoHomeCirculationVol. 121, No. 10How Would the Reverend Bayes Interpret High-Sensitivity Troponin? Free AccessEditorialPDF/EPUBAboutView PDFView EPUBSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessEditorialPDF/EPUBHow Would the Reverend Bayes Interpret High-Sensitivity Troponin? George A. Diamond and Sanjay Kaul George A. DiamondGeorge A. Diamond From the Division of Cardiology, Cedars-Sinai Medical Center, and the David Geffen School of Medicine, University of California, Los Angeles. and Sanjay KaulSanjay Kaul From the Division of Cardiology, Cedars-Sinai Medical Center, and the David Geffen School of Medicine, University of California, Los Angeles. Originally published1 Mar 2010https://doi.org/10.1161/CIR.0b013e3181d839e8Circulation. 2010;121:1172–1175Other version(s) of this articleYou are viewing the most recent version of this article. Previous versions: March 1, 2010: Previous Version 1 Deep down, we're all Bayesians, except sometimes when making mistakes.—I.J. Good, Good Thinking: The Foundations of Probability and its Applications.1Cardiac troponins are heavily relied on in the laboratory evaluation of patients with suspected myocardial infarction (MI) because of their putative high sensitivity and specificity for detection of myocardial necrosis. According to the National Academy of Clinical Biochemistry guidelines, "In the presence of a clinical history suggestive of acute coronary syndrome, maximal concentration of cardiac troponin exceeding the 99th percentile of values … for a reference control group on at least 1 occasion during the first 24 hour after the clinical event is considered indicative of myocardial necrosis consistent with myocardial infarction."2Article see p 1227Until recently, the commercially available troponin assays used in clinical practice lacked the stringent precision (10% coefficient of variation for levels below the 99th percentile cut-off) required by the guidelines.3 Over the past few years, however, so-called high-sensitivity, or ultrasensitive, assays have been developed that meet these requirements. Several recent studies have reported enhanced diagnostic and prognostic accuracy of these high-sensitivity troponin assays across a spectrum of patients with cardiovascular disease, including acute coronary syndromes (ACS),4,5 heart failure,6 and chronic stable coronary artery disease (CAD) without left ventricular systolic dysfunction.7In this issue of Circulation, Januzzi et al8 compare the diagnostic performance of a new high-sensitivity troponin T (hsTnT) assay with that of the conventional cardiac troponin T (cTnT) assay in a single-center cross-sectional study of 377 emergency room patients with chest pain and low-to-intermediate likelihood of ACS (MI or unstable angina). The reference diagnosis was based on the judgment of 2 physicians with access to all clinical and laboratory data, including the results of conventional serial troponin measurements and stress tests, through 6 months of follow-up. Comparisons were also made with anatomic findings from cardiac computed tomography with use of a 64-slice scanner. A key feature of the study was that the hsTnT assays, sampled once at a median of 4 hours from presentation at the time computed tomography was performed, were done solely for research purposes, and the results were not provided to the clinicians to guide patient treatment.Of the 377 patients enrolled (from a total of 1869 screened), 37 (9.8%) had an adjudicated final diagnosis of ACS—8 (2.1%) with acute MI and 29 (7.7%) with unstable angina. The remaining 340 patients (90.2%) had no evidence of active myocardial ischemia at the time of hospital discharge.The authors conclude that hsTnT provides superior overall diagnostic performance in comparison with cTnT. The greater accuracy of hsTnT for diagnosis of ACS was driven by its enhanced diagnostic sensitivity (from 35% to 62%) at the cost of a significant reduction in specificity (from 99% to 89%). As a result of this trade-off, hsTnT >13 pg/mL correctly detected 11 more cases than did cTnT >0.03 ng/mL among the 37 ACS patients, but it falsely detected 35 more cases among the 340 non-ACS patients. Elevations in hsTnT, nevertheless, "identified patients with significant structural heart disease irrespective of the diagnosis of ACS."Two noteworthy aspects of the current study deserve emphasis. First, in addition to conventional measures of diagnostic accuracy (sensitivity, specificity, and predictive accuracy) and strength of association (odds ratio), the authors also assessed the incremental discriminant accuracy of the new assay by comparing the C statistic (area under the receiver operating characteristic curve) for a prediction model using hsTnT with that for a prediction model using cTnT. The 0.05 gain in C statistic observed with hsTnT (from 0.74 to 0.79) failed to achieve statistical significance (P=0.28) but might yet be clinically important given the relative insensitivity of the C statistic for detecting moderately sized effects. For example, widely established cardiovascular risk factors such as systolic blood pressure and cholesterol are associated with small incremental gains in the C statistic (0.03 to 0.04) for the prediction of cardiovascular events.9 In performing these analyses, Januzzi et al used a diagnostic standard for the presence or absence of MI relative to hsTnT that considered all relevant clinical observations, including the results of cTnT.8 It is not clear how this choice affected the C statistic and other metrics of diagnostic accuracy reported by them.Nevertheless, the thoughtful clinician is more likely interested in the extent to which a biomarker correctly reclassifies individuals to a higher or lower risk of a specific outcome, especially if that reclassification has potentially important therapeutic implications. Such reclassification metrics depend heavily on the correlation matrix between hsTnT and cTnT and on the frequency and pattern of discordant observations. Unfortunately, these data are not presented in the current report. Thus, it remains to be established whether treatment of patients by the use of hsTnT is associated with an overall improvement in clinical outcome.The second noteworthy aspect of this study is the association of elevated hsTnT with prevalent cardiovascular disease as assessed by cardiac computed tomography. Nearly 11% (38 of 340) of patients without ACS also had elevations of hsTnT >13pg/mL. These patients were more likely to have risk factors or a previous history of CAD, a greater burden of CAD, larger cardiac chamber sizes, and greater left ventricular mass than were those without elevated hsTnT. This observation indicates that troponin, in addition to being a marker of ACS, might also be a marker of underlying structural heart disease, thereby supporting the use of hsTnT for cardiovascular screening. The mechanisms responsible for this association are unknown but might include silent myocardial ischemia, vascular inflammation, cardiomyocyte apoptosis, pressure and volume overload, and impairment of renal clearance.Whether elevations in hsTnT also identify a greater burden of cardiovascular disease in patients with ACS (as they do in those without ACS) is not directly apparent from this study. Furthermore, the investigators recently reported (in the same patients evaluated in this study) that both coronary artery plaque and stenosis detected by computed tomographic angiography predict ACS independently of cardiovascular risk factors or Thrombolysis in Myocardial Infarction risk score.10 Whether the predictive accuracy of hsTnT is improved when combined with cardiac computed tomography findings merits careful consideration.Although not directly tested by the investigators, an important advantage of the newer assays is in reliably ruling out MI early in the diagnostic process. For patients with suspected low likelihood of ACS, a single negative troponin level determined within 4 hours of presentation (having a negative predictive value in excess of 95%) would probably be sufficient to exclude ACS. On one hand, this holds promise of expediting the triage of patients with suspected ACS, thereby facilitating the process of appropriate healthcare delivery. On the other hand, the trade-off in clinical specificity for the diagnosis of ischemic myocardial injury might result in a substantially higher number of false-positive findings, especially when the pretest probability of ACS is low. This might be the case when sensitive assays are widely used in general clinical practice, not only in preselected patients in chest pain units or emergency rooms, as in the present study.Serial high-sensitivity troponin determinations (3 to 6 hours apart) might better define the kinetics of the release process11 and thereby improve discrimination of patients with acute myocardial injury (secondary to ischemia) from those with chronic injury (secondary to structural heart disease and other confounding conditions, such as myocarditis, acute heart failure, pulmonary embolism, and septic shock).2 Given the imperfect sensitivities and specificities resulting from these confounding conditions, therefore, even high-sensitivity troponin is best interpreted in conjunction with clinical and laboratory assessment by use of the Bayes' theorem.Bayesian Analysis of TroponinsDetermining whether or not a particular troponin elevation is due to ischemic myocardial injury is dependent on its pretest probability. Pretest probability for obstructive CAD has been formally quantified in reference to coronary angiography on the basis of observable clinical characteristics such as age, sex, risk factors, and the quality of presenting symptoms.12 Similarly, factors associated with a high pretest probability of ACS include a history of CAD or its risk factors, typical ischemic symptoms (rest or crescendo angina), ECG changes (ST depression of ≥1.0 mm or T wave inversion) and wall-motion abnormalities detected by noninvasive imaging.An ideal strategy for interpretation of troponin would define the patient-specific posttest probability of disease given the patient-specific pretest probability and the patient-specific observed troponin level. One such algorithm (based on clinical presentation, ECG changes, age, renal function, and cTnT) was recently shown to provide more accurate diagnosis of ACS13 but has not yet been prospectively validated.Consider a specific application of this approach. Suppose our patient has an hsTnT of 15 pg/mL. We can use the data in Table 2 of the article by Januzzi and colleagues to interpret this observation relative to a diagnosis of ACS by use of the Bayes' theorem. According to the data of Januzzi et al, the sensitivity for hsTnT >13 pg/mL is 62% and the specificity is 89% for ACS. Thus, if our patient has a pretest probability for ACS of 10% (based on clinical judgment or a formal algorithmic tool), Figure 1 shows the posttest probability of ACS given hsTnT >13 pg/mL to be 39% (consistent with the positive predictive value reported in Table 2 for an ACS prevalence of 9.4%). The figure also shows the corresponding posttest probabilities for positive cTnT levels by use of the >0.01 and >0.03 ng/mL cut-offs to be 64% and 80%, respectively—values that are higher than those for hsTnT. The difference in posttest probabilities becomes more pronounced at low pretest probabilities, highlighting the impact of low specificity of hsTnT in patients presenting with low pretest probability of ACS. By contrast, hsTnT delivers a posttest probability of ≥85% in patients with a pretest probability for ACS of ≥50%, illustrating that reduced specificity is of minor relevance in patients with intermediate to high pretest probability of ACS. Similar observations are apparent when the Bayes' theorem is applied to the diagnosis of MI or unstable angina. Download figureDownload PowerPointFigure 1. Bayesian analysis of acute coronary syndrome based on the sensitivity and specificity for troponin data provided by Januzzi et al.8 The top line is for cardiac troponin T (cTnT) >0.03 ng/mL, the middle line is for cTnT >0.01 ng/mL, and the bottom line is for high-sensitivity troponin T (hsTnT) >13 pg/mL.Thus, even very high values of troponin do not establish a diagnosis of ACS with confidence if the pretest probability is low.12 Conversely, very low values do not reliably exclude the diagnosis of ACS if pretest probability is high.12 From a Bayesian perspective, therefore, troponins are no different from any other imperfect diagnostic test, and even putative "high-sensitivity" assays must obey the mathematical laws of probability.Figure 2 illustrates the comparable analysis of hsTnT for diagnosis of acute MI in the current study by Januzzi et al8 and a previously reported study by Reichlin et al.4 Despite a higher-risk population enrolled in the study by Reichlin et al4 (prevalence of MI and ACS being 17% and 33%, respectively, versus 2.1% and 9.8% in the study by Januzzi et al), the posttest probability curves are virtually superimposed. The difference in posttest probabilities for MI in the 2 studies (11% versus 50%) despite comparable diagnostic accuracy highlights the impact of pretest probability on diagnostic interpretation. Download figureDownload PowerPointFigure 2. Bayesian analysis of acute myocardial infarction based on the sensitivity and specificity for high-sensitivity troponin T (hsTnT) data provided by Januzzi et al8 (top curve) and Reichlin et al4 (bottom curve) for the 99th percentile hsTnT cut-off. The post-test probabilities for a given pretest probability of 2.1% and 17% (prevalence of myocardial infarction in the 2 studies, respectively) are 11% and 50%.Just as a tool is only as good as its operator, a diagnostic test can be only as good as its interpretation. Expecting the test to provide all the answers without including the proper clinical context can lead to erroneous diagnoses. As our tests become more sophisticated so must our diagnostic interpretations. If we can appropriately control the process of diagnosis, we can appropriately control the process of treatment. And if we can appropriately control treatment, we can appropriately control the quality and cost of health care. The Bayes' theorem provides us with the appropriate language to exert this control.Future troponin research, therefore, should be directed (1) at developing and validating clinically relevant algorithms for estimating the pretest probability of various components of the composite diagnosis of ACS, (2) at characterizing the sensitivity and specificity of particular levels of troponin (in contrast to the open-ended cutpoints assessed by Januzzi et al) across the entire clinical spectrum of levels, and (3) at determining the optimal posttest probability thresholds for initiating appropriate therapeutic management strategies.In summary, although high-sensitivity troponin assays offer potential advantages over the conventional assays, the major problem with them, as with any other laboratory test, is often an inappropriate request and improper interpretation of the results, not the marker itself. Troponin evaluation should be performed only if clinically indicated, and elevated troponin should always be interpreted in the context of the clinical presentation. Only in this way can high-sensitivity troponin assays encourage optimal diagnosis, risk stratification, and patient treatment.The opinions expressed in this article are not necessarily those of the editors or of the American Heart Association.DisclosuresNone.FootnotesCorrespondence to George A. Diamond, MD, 2408 Wild Oak Drive, Los Angeles, CA 90068. E-mail [email protected] References 1 Good IJ. Good Thinking:The Foundations of Probability and its Applications. Minneapolis, Minn: University of Minnesota Press; 1983.Google Scholar2 Morrow DA, Cannon CP, Jesse RL, Newby LK, Ravkilde J, Storrow AB, Wu AHB, Christensen RH. National Academy of Clinical Biochemistry Laboratory Medicine Practice Guidelines: clinical characteristics and utilization of biochemical markers in acute coronary syndromes. Clin Chem. 2007; 53: 552–574.CrossrefMedlineGoogle Scholar3 Morrow DA. Clinical application of sensitive troponin assays. N Engl J Med. 2009; 361: 913–915.CrossrefMedlineGoogle Scholar4 Reichlin T, Hochholzer W, Bassetti S, Steuer S, Stelzig C, Hartwiger S, Biedert S, Schaub N, Buerge C, Potocki M, Noveanu M, Breidthardt T, Twerenbold R, Winkler K, Bingisser R, Mueller C. Early diagnosis of myocardial infarction with sensitive cardiac troponin assays. N Engl J Med. 2009; 361: 858–867.CrossrefMedlineGoogle Scholar5 Keller T, Zeller T, Peetz D, Tzikas S, Roth A, Czyz E, Bickel C, Baldus S, Warnholtz A, Fröhlich M, Sinning CR, Eleftheriadis MS, Wild PS, Schnabel RB, Lubos E, Jachmann N, Genth-Zotz S, Post F, Nicaud V, Tiret L, Lackner KJ, Münzel TF, Blankenberg S. Sensitive troponin I assay in early diagnosis of acute myocardial infarction. N Engl J Med. 2009; 361: 868–877.CrossrefMedlineGoogle Scholar6 Latini R, Masson S, Anand IS, Missov E, Carlson M, Vago T, Angelici L, Barlera S, Parrinello G, Maggioni AP, Tognoni G, Cohn JN. Val-HeFT Investigators. Prognostic value of very low plasma concentrations of troponin T in patients with stable chronic heart failure. Circulation. 2007; 116: 1242–1249.LinkGoogle Scholar7 Omland T, de Lemos JA, Sabatine MS, Christophi CA, Rice MM, Jablonski KA, Tjora S, Domanski MJ, Gersh BJ, Rouleau JL, Pfeffer MA, Braunwald E. Prevention of Events with Angiotensin Converting Enzyme Inhibition (PEACE) Trial Investigators. A sensitive cardiac troponin T assay in stable coronary artery disease. N Engl J Med. 2009; 361: 2538–2547.CrossrefMedlineGoogle Scholar8 Januzzi JL Jr, Bamberg F, Lee H, Truong QA, Nichols JH, Karakas M, Mohammed AA, Schlett CL, Nagurney JT, Hoffmann U, Koenig W. High-sensitivity troponin T concentrations in acute chest pain patients evaluated with cardiac computed tomography. Circulation. 2010; 121: 1227–1234.LinkGoogle Scholar9 Cook NR. Use and misuse of the receiver operating characteristic curve in risk prediction. Circulation. 2007; 115: 928–935.LinkGoogle Scholar10 Hoffmann U, Bamberg F, Chae CU, Nichols JH, Rogers IS, Seneviratne SK, Truong QA, Cury RC, Abbara S, Shapiro MD, Moloo J, Butler J, Ferencik M, Lee H, Jang IK, Parry BA, Brown DF, Udelson JE, Achenbach S, Brady TJ, Nagurney JT. Coronary computed tomography angiography for early triage of patients with acute chest pain: the ROMICAT (Rule Out Myocardial Infarction using Computer Assisted Tomography) trial. J Am Coll Cardiol. 2009; 53: 1642–1650.CrossrefMedlineGoogle Scholar11 Diamond GA, Kaul S. Hazardous to your health: kinetic foundations of risk stratification and therapeutic triage. Am J Med. 2006; 119: 275.e1–e6.Google Scholar12 Diamond GA, Forrester JS. Analysis of probability as an aid to the clinical diagnosis of coronary artery disease. N Engl J Med. 1979; 300: 1350–1358.CrossrefMedlineGoogle Scholar13 Alcalai R, Planer D, Culhaoglu A, Osman A, Pollak A, Lotan C. Acute coronary syndrome vs nonspecific troponin elevation: clinical predictors and survival analysis. Arch Intern Med. 2007; 167: 276–281.CrossrefMedlineGoogle Scholar Previous Back to top Next FiguresReferencesRelatedDetailsCited By Khan E, Lambrakis K, Nazir S, Chuang A, Halabi A, Tiver K, Briffa T, Cullen L, Horsfall M, French J, Sun B and Chew D (2022) Implementation of more sensitive cardiac troponin T assay in a state-wide health service, International Journal of Cardiology, 10.1016/j.ijcard.2021.11.013, 347, (66-72), Online publication date: 1-Jan-2022. T. Chakrapani A (2021) Biomarkers of Diseases: Their Role in Emergency Medicine Neurodegenerative Diseases - Molecular Mechanisms and Current Therapeutic Approaches, 10.5772/intechopen.94509 Sanfilippo F, Hillis G, Rankin J, Latchem D, Schultz C, Yong J, Li I and Briffa T (2020) Invasive Coronary Angiography after Chest Pain Presentations to Emergency Departments, International Journal of Environmental Research and Public Health, 10.3390/ijerph17249502, 17:24, (9502) McDonaugh B and Whyte M (2020) The Evolution and Future Direction of The Cardiac Biomarker, EMJ Cardiology, 10.33590/emjcardiol/20-00045 Chew D, Lambrakis K, Blyth A, Seshadri A, Edmonds M, Briffa T, Cullen L, Quinn S, Karnon J, Chuang A, Nelson A, Wright D, Horsfall M, Morton E, French J and Papendick C (2019) A Randomized Trial of a 1-Hour Troponin T Protocol in Suspected Acute Coronary Syndromes, Circulation, 140:19, (1543-1556), Online publication date: 5-Nov-2019. Zheng W, Ma J, Wu S, Wang G, Zhang H, Zheng J, Xu F, Wang J and Chen Y (2019) Effective combination of isolated symptom variables to help stratifying acute undifferentiated chest pain in the emergency department, Clinical Cardiology, 10.1002/clc.23170, 42:4, (467-475), Online publication date: 1-Apr-2019. Sandoval Y, Sharain K, Saenger A, Smith S, Apple F and Jaffe A Clinical use of cardiac troponin for acute cardiac care and emerging opportunities in the outpatient setting, Minerva Medica, 10.23736/S0026-4806.18.05874-3, 110:2 Robbins J and Gelfand E (2019) Unstable Angina and Non-ST Elevation Myocardial Infarction Comprehensive Cardiovascular Medicine in the Primary Care Setting, 10.1007/978-3-319-97622-8_11, (233-259), . Safdar B, Ong P and Camici P (2018) Identifying Myocardial Ischemia due to Coronary Microvascular Dysfunction in the Emergency Department: Introducing a New Paradigm in Acute Chest Pain Evaluation, Clinical Therapeutics, 10.1016/j.clinthera.2018.09.010, 40:11, (1920-1930), Online publication date: 1-Nov-2018. Summers S, Long B, April M, Koyfman A and Hunter C (2018) High sensitivity troponin: The Sisyphean pursuit of zero percent miss rate for acute coronary syndrome in the ED, The American Journal of Emergency Medicine, 10.1016/j.ajem.2018.03.075, 36:6, (1088-1097), Online publication date: 1-Jun-2018. Campbell A, Rodriguez A, Larson D, Strauss C, Garberich R, Partridge M, Henry T and Sharkey S (2018) Resource utilization and outcome among patients with selective versus nonselective troponin testing, American Heart Journal, 10.1016/j.ahj.2018.01.010, 199, (68-74), Online publication date: 1-May-2018. Blankenberg S and Zeller T (2018) Standard and Novel Biomarkers Chronic Coronary Artery Disease, 10.1016/B978-0-323-42880-4.00009-1, (98-113), . Morrow D (2017) Clinician's Guide to Early Rule-Out Strategies With High-Sensitivity Cardiac Troponin, Circulation, 135:17, (1612-1616), Online publication date: 25-Apr-2017. Brush J, Kaul S and Krumholz H (2016) Troponin Testing for Clinicians, Journal of the American College of Cardiology, 10.1016/j.jacc.2016.08.066, 68:21, (2365-2375), Online publication date: 1-Nov-2016. Chew D, Zeitz C, Worthley M, Grantham H, Beltrame J, Arstall M, Coates P, Astley C, Quinn S, Ratcliffe J, Horsfall M and Aylward P (2016) Randomized Comparison of High-Sensitivity Troponin Reporting in Undifferentiated Chest Pain Assessment, Circulation: Cardiovascular Quality and Outcomes, 9:5, (542-553), Online publication date: 1-Sep-2016. Ndrepepa G, Braun S, Cassese S, Mayer K, Lohaus R, Lahmann A, Fusaro M, Laugwitz K, Schunkert H and Kastrati A (2016) Valor pronóstico de la troponina T de alta sensibilidad tras intervención coronaria percutánea en pacientes con enfermedad coronaria estable, Revista Española de Cardiología, 10.1016/j.recesp.2016.02.023, 69:8, (746-753), Online publication date: 1-Aug-2016. Ndrepepa G, Braun S, Cassese S, Mayer K, Lohaus R, Lahmann A, Fusaro M, Laugwitz K, Schunkert H and Kastrati A (2016) Prognostic Value of High-sensitivity Troponin T After Percutaneous Coronary Intervention in Patients With Stable Coronary Artery Disease, Revista Española de Cardiología (English Edition), 10.1016/j.rec.2016.04.002, 69:8, (746-753), Online publication date: 1-Aug-2016. Li G, Wu X, Lu W, Cheng J, Wu X, Ai R, Zhou Z, Tang Z and Liao Y (2016) High-sensitivity cardiac troponin T: A biomarker for the early risk stratification of type-A acute aortic dissection?, Archives of Cardiovascular Diseases, 10.1016/j.acvd.2015.09.007, 109:3, (163-170), Online publication date: 1-Mar-2016. Than M and Cullen L (2016) Evaluation of Patients Presenting with Chest Pain in the Emergency Department: Where Do Troponins Fit In? Cardiac Biomarkers, 10.1007/978-3-319-42982-3_4, (41-55), . Sara J, Holmes D and Jaffe A (2015) Fundamental Concepts of Effective Troponin Use: Important Principles for Internists, The American Journal of Medicine, 10.1016/j.amjmed.2014.08.030, 128:2, (111-119), Online publication date: 1-Feb-2015. Chew D and Cullen L (2014) The promise of high‐sensitivity troponin testing, Medical Journal of Australia, 10.5694/mja14.00858, 201:3, (125-126), Online publication date: 1-Aug-2014. Biccard B (2014) Detection and management of perioperative myocardial ischemia, Current Opinion in Anaesthesiology, 10.1097/ACO.0000000000000071, 27:3, (336-343), Online publication date: 1-Jun-2014. Daniels L (2014) Making Sense of High Sensitivity Troponin Assays and their Role in Clinical Care, Current Cardiology Reports, 10.1007/s11886-014-0471-x, 16:4, Online publication date: 1-Apr-2014. Zeller T, Tunstall-Pedoe H, Saarela O, Ojeda F, Schnabel R, Tuovinen T, Woodward M, Struthers A, Hughes M, Kee F, Salomaa V, Kuulasmaa K and Blankenberg S (2013) High population prevalence of cardiac troponin I measured by a high-sensitivity assay and cardiovascular risk estimation: the MORGAM Biomarker Project Scottish Cohort, European Heart Journal, 10.1093/eurheartj/eht406, 35:5, (271-281), Online publication date: 1-Feb-2014. Pleister A, Selemon H, Elton S and Elton T (2013) Circulating miRNAs: novel biomarkers of acute coronary syndrome?, Biomarkers in Medicine, 10.2217/bmm.13.8, 7:2, (287-305), Online publication date: 1-Apr-2013. Newby L, Jesse R, Babb J, Christenson R, De Fer T, Diamond G, Fesmire F, Geraci S, Gersh B, Larsen G, Kaul S, McKay C, Philippides G, Weintraub W, Harrington R, Bhatt D, Anderson J, Bates E, Bridges C, Eisenberg M, Ferrari V, Fisher J, Garcia M, Gardner T, Gentile F, Gilson M, Hernandez A, Hlatky M, Jacobs A, Kaul S, Linderbaum J, Moliterno D, Mukherjee D, Rosenson R, Stein J, Weitz H and Wesley D (2012) ACCF 2012 Expert Consensus Document on Practical Clinical Considerations in the Interpretation of Troponin Elevations, Journal of the American College of Cardiology, 10.1016/j.jacc.2012.08.969, 60:23, (2427-2463), Online publication date: 1-Dec-2012. Hromádka M, Rajdl D, Trefil L, Racek J and Rokyta R (2012) Diagnostic sensitivity of high-sensitivity troponin T in acute myocardial infarction in patients with chest pain, Cor et Vasa, 10.1016/j.crvasa.2012.06.002, 54:7-8, (e227-e231), Online publication date: 1-Jul-2012. Jaffe A (2012) Troponin—Past, Present, and Future, Current Problems in Cardiology, 10.1016/j.cpcardiol.2012.02.002, 37:6, (209-228), Online publication date: 1-Jun-2012. Chew D (2012) National Heart Foundation Response to Letter, "Ambiguous Cardiac Troponin Recommendations", Heart, Lung and Circulation, 10.1016/j.hlc.2011.12.001, 21:3, (198), Online publication date: 1-Mar-2012. Mountain D and Brown A (2011) Chest pain research in Australasian emergency medicine: Putting our mark on the world stage, Emergency Medicine Australasia, 10.1111/j.1742-6723.2011.01457.x, 23:4, (395-397), Online publication date: 1-Aug-2011. Möckel M, Searle J, Danne O and Müller C (2011) Kardiale Biomarker in der NotfallmedizinCardiac biomarkers in emergency medicine, Notfall + Rettungsmedizin, 10.1007/s10049-010-1350-7, 14:3, (229-242), Online publication date: 1-Apr-2011. Grines C and Dixon S (2011) A Nail in the Coffin of Troponin Measurements After Percutaneous Coronary Intervention, Journal of the American College of Cardiology, 10.1016/j.jacc.2010.09.045, 57:6, (662-663), Online publication date: 1-Feb-2011. Christ M, Bertsch T, Popp S, Bahrmann P, Heppner H and Müller C High-sensitivity troponin assays in the evaluation of patients with acute chest pain in the emergency department, Clinical Chemistry and Laboratory Medicine (CCLM), 10.1515/CCLM.2011.695, 49:12 Kim J, Van Cott E and Lewandrowski K (2011) The Use of Decision Analysis Tools for the Selection of Clinical Laboratory Tests: Developing Diagnostic and Forecasting Models Using Laboratory Evidence Evidence Based Pathology and Laboratory Medicine, 10.1007/978-1-4419-1030-1_18, (305-322), . Omland T (2010) New features of troponin testing in different clinical settings, Journal of Internal Medicine, 10.1111/j.1365-2796.2010.02253.x, 268:3, (207-217) March 16, 2010Vol 121, Issue 10 Advertisement Article InformationMetrics https://doi.org/10.1161/CIR.0b013e3181d839e8PMID: 20194887 Originally publishedMarch 1, 2010 KeywordsEditorialsmyocardial infarctionepidemiologyPDF download Advertisement SubjectsDiagnostic Testing
Referência(s)