Evaluation of First-Draw Whole Blood, Point-of-Care Cardiac Markers in the Context of the Universal Definition of Myocardial Infarction
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1 Evaluation of First-Draw Whole Blood, Point-of-Care Cardiac Markers in the Context of the Universal Definition of Myocardial Infarction A Comparison of a Multimarker Panel to Troponin Alone and to Testing in the Central Laboratory Elizabeth Lee-Lewandrowski, PhD, MPH; James L. Januzzi Jr, MD; Ricky Grisson, MD, MBA; Asim A. Mohammed, MD; Grant Lewandrowski, BA; Kent Lewandrowski, MD N Context. Previous studies evaluating point-of-care testing (POCT) for cardiac biomarkers did not use current recommendations for troponin cutoff values or recognize the recent universal definition of acute myocardial infarction. Traditionally, achieving optimal sensitivity for the detection of myocardial injury on initial presentation required combining cardiac troponin and/or creatine kinase isoenzyme MB with an early marker, usually myoglobin. In recent years, the performance of central laboratory combining cardiac troponin assays has improved significantly, potentially obviating the need for a multimarker panel to achieve optimum sensitivity. Objective. To compare 2 commonly used POCT strategies to a fourth generation, central laboratory cardiac troponin T assay on first-draw specimens from patients being evaluated for acute myocardial infarction in the emergency department. The 2 strategies included a traditional POCT multimarker panel and a newer POCT method using cardiac troponin I alone. Design. Blood specimens from 204 patients presenting to the emergency department with signs and/or symptoms of Current guidelines for cardiac markers of myocardial necrosis recommend a total turnaround time of less than 1 hour and preferably less than 30 minutes. 1 This recommendation reflects the importance of rapid turnaround time to facilitate timely diagnosis and treatment of acute coronary syndrome (ACS). However, only a few Accepted for publication May 26, From the Departments of Pathology (Drs Grisson, Lee-Lewandrowski, and K. Lewandrowski and Mr G. Lewandrowski); and Cardiology (Drs Januzzi and Mohammed), Massachusetts General Hospital, Harvard Medical School, Boston. The authors have no relevant financial interest in the products or companies described in this article. This study was supported in part by a grant from Abbott Diagnostics, Chicago, Illinois. Dr Januzzi has received research grant support from Roche Diagnostics, Indianapolis, Indiana. Dr Lewandrowski has received research support from Biosite Diagnostics. Reprints: Kent Lewandrowski, MD, Department of Pathology, Massachusetts General Hospital, 55 Fruit St, Gray 5 Chemistry, Boston, MA ( klewandrowski@partners.org). myocardial ischemia were measured on the 2 POCT systems and by a central laboratory method. The diagnosis for each patient was determined by retrospective chart review. Results. The cardiac troponin T assasy alone was more sensitive for acute myocardial infarction than the multimarker POCT panel with equal or better specificity. When compared with a POCT troponin I, the cardiac troponin T was also more sensitive, but this difference was not significant. The POCT troponin I alone also had the same sensitivity as the multimarker panel. Conclusions. Testing for combining cardiac troponin alone using newer, commercially available, central laboratory or POCT assays performed with equal or greater sensitivity to acute myocardial infarction as the older, traditional, multimarker panel. In the near future, highsensitivity, central laboratory troponins will be available for routine clinical use. As a result, the quality gap between central laboratories and older POCT methods will continue to widen, unless the performance of the POCT methods is improved. (Arch Pathol Lab Med. 2011;135: ) hospitals have been able to meet the less-than-60-minute standard. 2 Recognition of this problem has prompted some institutions to perform rapid point-of-care testing for cardiac markers in the emergency department (ED). 3 Studies have shown that implementation of point-of-care testing (POCT) for cardiac markers may improve ED operations and decrease patient length of stay. 4,5 Presumably, this results from the shorter turnaround time required for whole blood, POCT assays. For example, implementation of POCT for cardiac markers in our institution reduced turnaround time by 93 minutes, compared with that of the central laboratory. 4 Testing may include various combinations of cardiac-specific troponin (ctn) I or T, creatine kinase isoenzyme MB (CK-MB), and myoglobin (MYO) and multimarker panels (ctn, CK-MB, and MYO). Several studies have reported on the analytic performance of POCT for markers of myocardial injury. 6 Most of these studies were conducted some years ago and do not Arch Pathol Lab Med Vol 135, April 2011 Point-of-Care Cardiac Markers Lee-Lewandrowski et al 459
2 reflect the current state of analytic technologies for these markers. Among the more recent studies, one report evaluated the i-stat ctni as a tool for risk stratification of patients in the ED, without a comparison to the clinical laboratory, 7 and another compared the i-stat ctni to a central laboratory analyzer but did not include a multimarker panel. 8 In recent years, the analytic performance of standard central laboratory testing for ctn has improved substantially, resulting in assays with improved low-end sensitivity, 9 and new approaches for reporting ctni or ctnt are now endorsed. 1,2 As an example, current consensus recommendations endorse a ctn cutoff at the 99th percentile of the reference population if the assays have less than a 10% coefficient of variation (CV) at that cutoff point. 1,9,10 Moreover, at least one major consensus panel has stated that assays that do not have independent validation of optimal imprecision (CV # 10%) are not recommended. 1 This creates a necessary tension between recommendations for both rapid turnaround times and high precision plus excellent low-end sensitivity, characteristics not widely shared by POCT methods. Another major development has been the creation of new criteria for the diagnosis of acute myocardial infarction (AMI) and a new classification system for AMI. 10,11 Collectively, these developments have rendered many older studies on the performance of POCT cardiac markers obsolete. Various approaches have been employed for the assessment of patients presenting to the emergency department with signs and symptoms suggestive of an acute coronary syndrome Beyond securing an accurate diagnosis, an important component in the evaluation of patients with possible ACS is to make rapid decisions concerning emergent treatment and to determine disposition to an appropriate care setting (eg, observation unit, cardiac intensive care unit). For this reason, the first-draw specimen for cardiac marker testing is particularly important 15 because the results of this testing have significant influence on emergent treatment decisions. In the current study, we evaluated the performance of 2 commonly used POCT devices for cardiac markers using first-draw specimens in the ED with a comparison to an automated ctnt performed in the central laboratory. The ctn assays were evaluated using a cutoff set at the 99th percentile. The 2 POCT technologies included a multimarker panel and the other ctni alone. The major questions we chose to address in this study were the following: 1. Do commonly used, POCT, whole blood, cardiac marker assays continue to perform in a clinically acceptable manner compared with currently available central laboratory assays using current recommendations for reporting of marker cutoff values and AMI definitions? 2. Can current ctn assays achieve equivalent sensitivity for AMI on first-draw specimens when compared with a multimarker panel? 3. Can a combination of 2 different ctns, taken together as a panel (I and T), achieve greater sensitivity for AMI on first-draw specimens than a single ctn alone? MATERIALS AND METHODS Study Protocol The Massachusetts General Hospital is an 898-bed, urban, tertiary-care, academic medical center located in Boston. The 204 patients enrolled in this study were obtained through continuous, convenience sampling of patients presenting to the Massachusetts General Hospital ED with signs and symptoms of an ACS between February 17, 2009, and February 20, 2009, and between March 3, 2009, and March 18, Common presenting signs and symptoms included, but were not limited to, resting or exertional chest pain; arm, shoulder, or jaw pain; exertional dyspnea; palpitations; syncope; nausea and/or diaphoresis; and new, electrocardiogram abnormalities. Venous whole blood was collected from each patient by the Massachusetts General Hospital ED staff in 3-mL Vacutainer tubes (gel-barrier, lithium heparin, and potassium ethylenediaminetetraacetic acid; Becton Dickenson, Franklin Lakes, New Jersey). As a part of the clinical evaluation of these patients, whole blood (ethylenediaminetetraacetic acid) testing for ctni and CK-MB was performed by trained medical technologists in the ED using the Inverness/Biosite Triage cardiac reader instrument (Inverness/Biosite Inc, San Diego, California) and, in selected cases, measurement for ctnt using ethylenediaminetetraacetic acid plasma samples in the central laboratory. The Inverness/Biosite instrument also measures MYO, which was used in this study, but these results are not reported in our institution for clinical purposes. As part of the study protocol, heparinized whole blood specimens were also measured for ctni in the ED using the i-stat instrument (Abbott Diagnostics, Chicago, Illinois), but these test results were not reported to clinicians. For cases in which ctnt was not requested in the ED, blood samples were retrieved from the emergency department and measured for ctnt using the Elecsys E170 immunoassay analyzer (fourth generation ctnt, Roche Diagnostics, Indianapolis, Indiana). These results were also not reported to clinicians. Using the available laboratory data, electrocardiographic results, and clinical findings, ED physicians or, in the case of admitted patients, inpatient, hospital-based physicians, determined the final diagnosis. Medical records were reviewed for all 204 patients by 2 of the authors (K.L., R.G.). In cases where there was any question as to the occurrence of an ACS, the medical records were reviewed by a clinical cardiologist (J.L.J.). Acute myocardial infarction (MI) was judged as type 1 (spontaneous) or type 2 (supply-demand ischemia) per current consensus. 10 Current recommendations for the reporting of ctn suggest that the upper reference limit be set at the 99th percentile of the reference population. At this point, the assay should have a coefficient of variation (CV) of less than or equal to 10%. Using that recommendation, the respective 99th percentile values for the 3 ctns used in this study are the following: for the Abbott i- STAT, 0.08 mg/l (10% CV mg/l); for the Inverness/Biosite reader,,0.05 mg/l (10% CV, not available, see below); and for the Roche Elecsys 2010,,0.03 mg/l (10% CV ). The cutoff for the Inverness/Biosite troponin results requires specific comment. The manufacturer s package insert recommends a troponin I diagnostic cutoff #0.39 mg/l. The manufacturer also reports a 99th percentile of 0.05 mg/l. However, the CV at this troponin concentration is much greater than 10% and has not been independently validated. For these reasons, the 99th percentile cutoff on the Inverness/Biosite Triage does not meet acceptable guidelines. Because of this ambiguity, we chose to evaluate the Inverness/Biosite ctni at both cutoff points (#0.39 mg/l and 0.05 mg/l). For the Inverness/Biosite multimarker panel, we used cutoff values of less than or equal to 7.4 mg/l for CK-MB and less than 170 mg/l for MYO. This protocol was approved by the Massachusetts General Hospital Institutional Review Board. Statistical Methods Standard measures of diagnostic accuracy, including sensitivity, specificity, positive predictive value, and negative predictive value were calculated for each individual cardiac biomarker approach (multimarker panel, ctni, CK-MB, and MYO; i-stat, point-of-care ctni; and Elecsys, ctnt). A statistical analysis of the comparative performance of the 3 approaches was evaluated using 2-sided Z test statistics assessing the difference among proportions. 460 Arch Pathol Lab Med Vol 135, April 2011 Point-of-Care Cardiac Markers Lee-Lewandrowski et al
3 Table 1. Performance of 3 Cardiac Marker Approaches for Detecting Acute Myocardial Infarction on First-Draw Specimens in the Emergency Department Cardiac Marker Assay Sensitivity Specificity PPV NPV 1. MMP using manufacturer-suggested ctni cutoff MMP using manufacturer s 99th percentile cutoff for ctni i-stat ctni Elecsys ctnt Abbreviations: ctni, cardiac troponin I; ctnt, cardiac troponin T; MMP, multimarker panel; NPV, negative predictive value; PPV, positive predictive value. RESULTS Of the 204 patients in the study, there were 22 cases (10.8%) of AMI identified in the study. There were 110 men (53.9%; mean age, 61.7 years) and 94 women (46.1%; mean age, 68.6 years). Of the 204 patients in the study, 136 (66.7%) were admitted to the hospital, 22 (10.8%) were admitted to the observation unit, and 46 (22.5%) were discharged home from the ED. Of the 22 cases of AMI, there were 13 cases (59%) of type 1 MI, (of which, 11 [85%] were non-st elevated MIs, and 2 [15%] were ST-elevated MIs) and 9 cases (41%) of type 2 MI. Table 1 shows the relative performance of the 3 testing options (POCT multimarker panel, POCT ctni, and central laboratory ctnt) for detecting patients with types 1 and 2 AMI on the first-draw specimen in the ED. Using the Inverness/Biosite Triage system, the ctni cutoff recommended in the manufacturer s package insert (2008 copyright version) is #0.39 mg/l. However, as stated previously, this 99th percentile cutoff exhibits a CV greater than 10% and does not meet established guidelines. For this reason, the analysis comparing the Inverness/Biosite multimarker panel to the other 2 approaches required an evaluation of the Inverness/ Biosite ctni using 2 different cutoffs. Overall, the sensitivity of the 3 approaches for AMI was 55% or 83% (for the multimarker panel using the manufacturer s suggested troponin cutoff or the presumed 99th percentile troponin cutoff), 63% (i-stat ctni), and 88% (central laboratory ctnt), respectively. However, there was no statistically significant difference among these 3 approaches, as shown in Table 2, with the exception of the multimarker protocol using the manufacturer s suggested ctni cutoff, which was statistically less sensitive than the central laboratory fourth generation ctnt. The i-stat ctni was statistically more specific than the Inverness/Biosite multimarker panel, irrespective of the cutoff point used, and was more specific than the central laboratory fourth generation ctnt. The explanation for this improved specificity is not known. All 3 methods exhibited a high negative predictive value (.95%) but a relatively low positive predictive value (34% 58%; Table 2). In summary, the central laboratory fourth generation ctnt performed with equal or better sensitivity and specificity than the multimarker panel did, depending on the Inverness/Biosite ctni cutoff used. The sensitivity of the central laboratory ctnt was not significantly better than that of the i-stat ctni, although the i-stat was statistically more specific. Table 3 shows a receiver operator characteristic curve analysis for the 3 cardiac marker approaches to the diagnosis of AMI. The area under the curve for MYO was only The Inverness/Biosite CK-MB had a slightly higher area under the curve, when compared with the Inverness/Biosite ctni, whereas the i-stat ctni had an area under the curve similar to that of the central laboratory ctnt. The relative value of adding CK-MB or MYO to the Inverness/Biosite multimarker panel is illustrated by an analysis of which markers were positive in patients with AMI and whether any of the markers were uniquely positive for any individual patient, as shown in Table 4. Both ctni and MYO were uniquely positive on selected patients with AMI, but CK-MB was never positive when the other 2 markers were negative, suggesting that CK-MB adds no improvement in sensitivity to the panel. Combining 2 different ctns did not improve overall sensitivity (ctnt plus Inverness/Biosite, 88%; ctnt plus i- STAT, 88%) indicating that a multitroponin panel provides no improvement in sensitivity. COMMENT A major development in the field of biomarker testing for AMI diagnosis includes consensus recommendations for assay performance, 1 as well as a new classification system for AMI Specifically, the latter includes 5 types of MI, which include spontaneous syndromes (type 1); infarction secondary to ischemia from increased oxygen demand (also called demand ischemia) or decreased supply (type 2); sudden, unexpected cardiac death (type 3); and MI associated with various procedures (types 4a and 4b and type 5). 11 Collectively, these developments have rendered many older studies on the performance of POCT cardiac markers obsolete, and such studies need to be reconsidered in the modern era of redefined MI. Various approaches have been employed for assessing patients presenting to the ED with signs and symptoms suggestive of an ACS. Among these is the use of multimarker POCT panels (eg, TnI, CK-MB, and MYO) and accelerated, rule-out protocols that use repeated testing for cardiac markers during a short timeframe Beyond securing an accurate diagnosis, an important component in the evaluation of patients with possible ACS is to make rapid decisions concerning emergent treatment and to determine disposition to an appropriate care setting (eg, observation unit, cardiac intensive care unit). For this reason, the first-draw specimen for cardiac marker testing is particularly important. 15 Although it is well recognized that a single, first-draw specimen is insufficient to rule out MI, the results of this test have a significant influence on emergent treatment decisions. In a previous study, 15 we reported that only 63% of patients with an MI exhibited a positive cardiac marker on the firstdraw specimen using a multimarker approach with an older, qualitative, POCT cardiac marker technology (with a specificity of 81%). In the present study, we compared commonly used, whole blood cardiac marker POCT assays to an automated Arch Pathol Lab Med Vol 135, April 2011 Point-of-Care Cardiac Markers Lee-Lewandrowski et al 461
4 Table 2. Statistical Comparison of 3 Cardiac Marker Approaches for Detecting Acute Myocardial Infarction on First- Draw Specimens in the Emergency Department Cardiac Marker Assay P Value Comment Sensitivity 1. MMP using manufacturer-suggested ctni cutoff to i-stat ctni.54 NS 2. MMP using manufacturer s 99th percentile ctni cutoff to i-stat ctni.18 NS 3. MMP using manufacturer-suggested ctni cutoff to ctnt.02 S 4. MMP using manufacturer s 99th percentile ctni cutoff to ctnt.68 NS 5. i-stat ctni to ctnt.08 NS Specificity 1. MMP using manufacturer-suggested ctni cutoff to i-stat ctni,.001 S 2. MMP using manufacturer s 99th percentile ctni cutoff to i-stat ctni,.001 S 3. MMP using manufacturer-suggested ctni cutoff to ctnt.13 NS 4. MMP using manufacturer s 99th percentile ctni cutoff to ctnt.03 S 5. i-stat ctni to ctnt.02 S Abbreviations: ctni, cardiac troponin I; ctnt, cardiac troponin T; MMP, multimarker panel; NS, not significant; S, significant. central laboratory ctnt assay on first-draw specimens, using the recommended cutoff of the 99th percentile of the reference range and the criteria for AMI proposed in the new universal classification. The major findings of this study include the following: 1. The central laboratory ctnt assay performed with equal or better sensitivity and specificity for detecting AMI on first-draw specimens compared to the POCT, multimarker approach, combining a ctni assay with CK-MB and MYO. The difference in sensitivity between the ctnt was not significantly better than the i-stat ctni, although the i-stat was statistically more specific. The sensitivity of the i-stat ctni assay was not statistically different from the multimarker approach using either Inverness/Biosite troponin cutoff, but the i-stat ctni assay was more specific than the multimarker panel, and overall the Inverness/Biosite multimarker panel provided less-robust performance. 2. The CK-MB added no additional sensitivity to the Inverness/Biosite multimarker panel beyond that offered by the combination of ctni and MYO. 3. Combining results from 2 different ctns did not improve overall sensitivity. The Roche fourth generation ctnt alone performed with greater sensitivity for AMI than the POCT multimarker panel. It is expected that, with further development of high-sensitivity ctn methods, which allow the 99th percentile to be used and demonstrate excellent sensitivity for the diagnosis of MI, 16 this quality gap between automated assays and POCT methods will continue to widen, unless POCT technology improves. As POCT is typically the first test run on patients Table 3. Receiver Operator Characteristic Analysis of 3 Cardiac Marker Approaches for the Detection of Acute Myocardial Infarction Approach, mg/l Area Under the Curve 95% Confidence Interval Inverness/Biosite ctni, Inverness/Biosite CK-MB, Inverness/Biosite MYO, i-stat ctni, ctnt, Abbreviations: CK-MB, creatine kinase isoenzyme MB; ctni, cardiac troponin I; ctnt, cardiac troponin T; MYO, myoglobin. presenting to the ED with suspected ACS, this is of great concern and should be a significant consideration for future design of POCT methods. In our study, we recognized the distinction between type 1 and 2 MIs. It is noteworthy that 9 of the 22 AMIs (41%) in our study were attributed to demand ischemia. Many of these cases, and some of the type 1 AMIs, exhibited first-draw ctn values well below prior upper reference limits (eg, 0.10 ng/ml for ctnt ) and, therefore, may not have been included as patients with MIs in earlier studies. For this reason, older studies comparing POCT devices to less-sensitive, earlier generation, central laboratory ctn assays must be reevaluated in view of the changing performance characteristics of the assays. The availability in the near future of so-called high-sensitivity troponin assays will necessitate even further evaluation. The conclusions above should be understood in the context of an important caveat. These results reflect the performance of various assays on first-draw specimens in the ED. The first-draw specimen is important because it aids in rapid triage and initial treatment of patients with suspected ACS. However, it is well recognized that a single specimen for cardiac markers is not sufficient to rule out an AMI and that serial markers are required for this purpose. Our data do not indicate whether either of the 3 approaches studied are preferable to the others for ruling out AMIs using serial marker values. Rather, our results indicate the relative performance of the 3 approaches to support clinical decision-making when the patient first presents to the ED. The apparently better performance of the fourth generation ctnt assay, when compared with the multimarker panel, must be understood within the context of the turnaround time that is typically available from the central laboratory. Many central laboratories cannot meet the recommended goal for turnaround time in cardiac marker testing. Emergency department physicians must, therefore, balance the need Table 4. Utility of Individual Markers for Detection of Acute Myocardial Infarction in the Multimarker Panel Utility TnI, 0.39 mg/l TnI, 99th Percentile CK-MB # 7.4 mg/l MYO, 170 mg/l % Positive % Uniquely positive Abbreviations: CK-MB, creatine kinase isoenzyme MB; TnI, troponin I; MYO, myoglobin. 462 Arch Pathol Lab Med Vol 135, April 2011 Point-of-Care Cardiac Markers Lee-Lewandrowski et al
5 for rapid cardiac marker results against the relative analytic performance of the different methods. This study was supported in part by a grant from Abbott Diagnostics, Chicago, Illinois. References 1. Braunwald E, Antman EM, Beasley JW, et al. ACC/AHA guidelines for the management of patients with unstable angina and non-st segment elevation myocardial infarction: a report of the American College of Cardiology/American Heart Association task force on practice guidelines (Committee on the Management of Patients With Unstable Angina) executive summary and recommendations. Circulation. 2000:102(10); Apple FS, Jesse RL, Newby LK, et al; IFCC Committee for Standardization of Markers of Cardiac Damage; National Academy of Clinical Biochemistry. National Academy of Clinical Biochemistry and IFCC Committee for Standardization of Markers of Cardiac Damage laboratory medicine practice guidelines: analytical issues for biochemical markers of acute coronary syndromes. Clin Chem. 2007;53(4): Lewandrowski K. Point-of-care testing for cardiac markers in acute coronary syndromes and heart failure. Clin Lab Med. 2009;29(3); Lee-Lewandrowski E, Corboy D, Lewandrowski K, Sinclair J, McDermot S, Benzer TI. Implementation of a point-of-care satellite laboratory in the emergency department of an academic medical center: impact on test turnaround time and patient emergency department length of stay. Arch Pathol Lab Med. 2003;127(4): Storrow AB, Lyon JA, Porter MW, Zhou C, Han JH, Lindsell CJ. A systematic review of emergency department point-of-care cardiac markers and efficiency measures. Point Care. 2009:8(3); Collinson PO. Testing for cardiac markers at the point of care. Clin Lab Med. 2001;21(2): Apple FS, Ler R, Chung AY, Berger MJ, Murakami MM. Point-of-care i-stat cardiac troponin I for assessment of patients with symptoms suggestive of acute coronary syndrome. Clin Chem. 2006;52(2): Bock JL, Singer AJ, Thode HC Jr. Comparison of emergency department patient classification by point-of-care and central laboratory methods for cardiac troponin I. Am J Clin Pathol. 2008;130(1): Apple FS, Pearce LA, Smith SW, Kaczmarek JM, Murakami MM. Role of monitoring changes in sensitive cardiac troponin I assay results for early diagnosis of myocardial infarction and prediction of risk of adverse events. Clin Chem. 2009;55(5): Alpert JS, Thygesen K, Antman E, Bassand JP; Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction. Myocardial infarction redefined: a consensus document of the Joint European Society of Cardiology/American College of Cardiology Committee for the Redefinition of Myocardial Infarction. J Am Coll Cardiol. 2000;36(3): Thygesen K, Alpert JS, White HD, et al; Joint European Society of Cardiology/American College of Cardiology/American Heart Association/World Heart Federation Task Force for the Redefinition of Myocardial Infarction. Universal definition of myocardial infarction. Circulation. 2007;116: Ng SM, Krishnaswamy P, Morissey R, Clopton P, Fitzgerald R, Maisel A. Ninety-minute accelerated critical pathway for chest pain evaluation. Am J Cardiol. 2001;88(6): Dadkhah S, Sharain K, Sharain R, et al. The value of bedside cardiac multibiomarker assay in rapid and accurate diagnosis of acute coronary syndromes. Crit Pathw Cardiol. 2007;6(2): McCord J, Nowak RM, McCullough PA, et al. Ninety minute exclusion of acute myocardial infarction by use of quantitative point-of-care testing of myoglobin and troponin I. Circulation. 2001;104(13): Kratz A, Januzzi JL, Lewandrowski KB, Lee-Lewandrowski E. Positive predictive value of a point-of-care testing strategy on first-draw specimens for the emergency department-based detection of acute coronary syndromes. Arch Pathol Lab Med. 2002;126(12): Reichlin T, Hochholzer W, Bassetti S, et al. Early diagnosis of myocardial infarction with sensitive cardiac troponin assays. N Engl J Med. 2009;361(9): Arch Pathol Lab Med Vol 135, April 2011 Point-of-Care Cardiac Markers Lee-Lewandrowski et al 463
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