Peter A Kavsak1, Johannes T Neumann2, Louise Cullen2, Martin Than2, Colleen Shortt2, Jaimi H Greenslade2, John W Pickering2, Francisco Ojeda2, Jinhui Ma2, Natasha Clayton2, Jonathan Sherbino2, Stephen A Hill2, Matthew McQueen2, Dirk Westermann2, Nils A Sörensen2, William A Parsonage2, Lauren Griffith2, Shamir R Mehta2, P J Devereaux2, Mark Richards2, Richard Troughton2, Chris Pemberton2, Sally Aldous2, Stefan Blankenberg2, Andrew Worster2. 1. Departments of Pathology and Molecular Medicine (Kavsak, Hill, McQueen), Health Research Methods, Evidence and Impact (Ma, Griffith); and Medicine (Clayton); Division of Emergency Medicine (Shortt, Sherbino, Worster); Division of Cardiology (Mehta, Devereaux); Population Health Research Institute (Devereaux), McMaster University, Hamilton, Ont.; Department of General and Interventional Cardiology (Neumann, Ojeda, Westermann, Sörensen, Blankenberg), University Heart Center Hamburg Eppendorf, Hamburg, Germany; Royal Brisbane and Women's Hospital (Cullen, Greenslade, Parsonage), Brisbane, Australia; Christchurch Hospital (Than, Pickering, Troughton, Aldous), Christchurch, New Zealand; Department of Medicine and Christchurch Heart Institute, University of Otago (Richards, Pickering, Troughton, Pemberton), Christchurch, New Zealand; Cardiovascular Research Institute (Richards), National University of Singapore kavsakp@mcmaster.ca. 2. Departments of Pathology and Molecular Medicine (Kavsak, Hill, McQueen), Health Research Methods, Evidence and Impact (Ma, Griffith); and Medicine (Clayton); Division of Emergency Medicine (Shortt, Sherbino, Worster); Division of Cardiology (Mehta, Devereaux); Population Health Research Institute (Devereaux), McMaster University, Hamilton, Ont.; Department of General and Interventional Cardiology (Neumann, Ojeda, Westermann, Sörensen, Blankenberg), University Heart Center Hamburg Eppendorf, Hamburg, Germany; Royal Brisbane and Women's Hospital (Cullen, Greenslade, Parsonage), Brisbane, Australia; Christchurch Hospital (Than, Pickering, Troughton, Aldous), Christchurch, New Zealand; Department of Medicine and Christchurch Heart Institute, University of Otago (Richards, Pickering, Troughton, Pemberton), Christchurch, New Zealand; Cardiovascular Research Institute (Richards), National University of Singapore.
Abstract
BACKGROUND: Testing for high-sensitivity cardiac troponin (hs-cTn) may assist triage and clinical decision-making in patients presenting to the emergency department with symptoms of acute coronary syndrome; however, this could result in the misclassification of risk because of analytical variation or laboratory error. We sought to evaluate a new laboratory-based risk-stratification tool that incorporates tests for hs-cTn, glucose level and estimated glomerular filtration rate to identify patients at risk of myocardial infarction or death when presenting to the emergency department. METHODS: We constructed the clinical chemistry score (CCS) (range 0-5 points) and validated it as a predictor of 30-day myocardial infarction (MI) or death using data from 4 cohort studies involving patients who presented to the emergency department with symptoms suggestive of acute coronary syndrome. We calculated diagnostic parameters for the CCS score separately using high-sensitivity cardiac troponin I (hs-cTnI) and high-sensitivity cardiac troponin T (hs-cTnT). RESULTS: For the combined cohorts (n = 4245), 17.1% of participants had an MI or died within 30 days. A CCS score of 0 points best identified low-risk participants: the hs-cTnI CCS had a sensitivity of 100% (95% confidence interval [CI] 99.5%-100%), with 8.9% (95% CI 8.1%-9.8%) of the population classified as being at low risk of MI or death within 30 days; the hs-cTnT CCS had a sensitivity of 99.9% (95% CI 99.2%-100%), with 10.5% (95% CI 9.6%-11.4%) of the population classified as being at low risk. The CCS had better sensitivity than hs-cTn alone (hs-cTnI < 5 ng/L: 96.6%, 95% CI 95.0%-97.8%; hs-cTnT < 6 ng/L: 98.2%, 95% CI 97.0%-99.0%). A CCS score of 5 points best identified patients at high risk (hs-cTnI CCS: specificity 96.6%, 95% CI 96.0%-97.2%; 11.2% [95% CI 10.3%-12.2%] of the population classified as being at high risk; hs-cTnT CCS: specificity 94.0%, 95% CI 93.1%-94.7%; 13.1% [95% CI 12.1%-14.1%] of the population classified as being at high risk) compared with using the overall 99th percentiles for the hs-cTn assays (specificity of hs-cTnI 93.2%, 95% CI 92.3-94.0; specificity of hs-cTnT 73.8%, 95% CI 72.3-75.2). INTERPRETATION: The CCS score at the chosen cut-offs was more sensitive and specific than hs-cTn alone for risk stratification of patients presenting to the emergency department with suspected acute coronary syndrome. Study registration: ClinicalTrials.gov, nos. NCT01994577; NCT02355457.
BACKGROUND: Testing for high-sensitivity cardiac troponin (hs-cTn) may assist triage and clinical decision-making in patients presenting to the emergency department with symptoms of acute coronary syndrome; however, this could result in the misclassification of risk because of analytical variation or laboratory error. We sought to evaluate a new laboratory-based risk-stratification tool that incorporates tests for hs-cTn, glucose level and estimated glomerular filtration rate to identify patients at risk of myocardial infarction or death when presenting to the emergency department. METHODS: We constructed the clinical chemistry score (CCS) (range 0-5 points) and validated it as a predictor of 30-day myocardial infarction (MI) or death using data from 4 cohort studies involving patients who presented to the emergency department with symptoms suggestive of acute coronary syndrome. We calculated diagnostic parameters for the CCS score separately using high-sensitivity cardiac troponin I (hs-cTnI) and high-sensitivity cardiac troponin T (hs-cTnT). RESULTS: For the combined cohorts (n = 4245), 17.1% of participants had an MI or died within 30 days. A CCS score of 0 points best identified low-risk participants: the hs-cTnI CCS had a sensitivity of 100% (95% confidence interval [CI] 99.5%-100%), with 8.9% (95% CI 8.1%-9.8%) of the population classified as being at low risk of MI or death within 30 days; the hs-cTnT CCS had a sensitivity of 99.9% (95% CI 99.2%-100%), with 10.5% (95% CI 9.6%-11.4%) of the population classified as being at low risk. The CCS had better sensitivity than hs-cTn alone (hs-cTnI < 5 ng/L: 96.6%, 95% CI 95.0%-97.8%; hs-cTnT < 6 ng/L: 98.2%, 95% CI 97.0%-99.0%). A CCS score of 5 points best identified patients at high risk (hs-cTnI CCS: specificity 96.6%, 95% CI 96.0%-97.2%; 11.2% [95% CI 10.3%-12.2%] of the population classified as being at high risk; hs-cTnT CCS: specificity 94.0%, 95% CI 93.1%-94.7%; 13.1% [95% CI 12.1%-14.1%] of the population classified as being at high risk) compared with using the overall 99th percentiles for the hs-cTn assays (specificity of hs-cTnI 93.2%, 95% CI 92.3-94.0; specificity of hs-cTnT 73.8%, 95% CI 72.3-75.2). INTERPRETATION: The CCS score at the chosen cut-offs was more sensitive and specific than hs-cTn alone for risk stratification of patients presenting to the emergency department with suspected acute coronary syndrome. Study registration: ClinicalTrials.gov, nos. NCT01994577; NCT02355457.
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