Michael J Lipinski1, Nevin C Baker1, Ricardo O Escárcega1, Rebecca Torguson1, Fang Chen1, Sally J Aldous2, Michael Christ3, Paul O Collinson4, Steve W Goodacre5, Johannes Mair6, Kenji Inoue7, Ulrich Lotze8, Mustapha Sebbane9, Jean-Paul Cristol10, Yonathan Freund11, Camille Chenevier-Gobeaux12, Christophe Meune13, Kai M Eggers14, Radosław Pracoń15, Donald H Schreiber16, Alan H B Wu17, Jordi Ordoñez-Llanos18, Allan S Jaffe19, Raphael Twerenbold20, Christian Mueller21, Ron Waksman22. 1. MedStar Cardiovascular Research Network, MedStar Heart Institute, Medstar Washington Hospital Center, Washington, DC. 2. Department of Cardiology, Christchurch Hospital, Christchurch, New Zealand. 3. Department of Emergency and Critical Care Medicine, Paracelsus Medical University, Nuremberg, Germany. 4. Clinical Blood Sciences Laboratory, St George's Hospital, London, United Kingdom. 5. School of Health and Related Research, University of Sheffield, Sheffield, United Kingdom. 6. Department of Internal Medicine, Innsbruck Medical University, Innsbruck, Austria. 7. Department of Cardiology, Juntendo University Nerima Hospital, Tokyo, Japan. 8. Department of Internal Medicine, DRK-Manniske-Krankenhaus Bad Frankenhausen, Frankenhausen, Germany. 9. Départment des urgences, Centre Hospitalier Régional Universitaire Lapeyronie, Montpellier, France. 10. Département de Biochimie, Centre Hospitalier Régional Universitaire Lapeyronie, Montpellier, France. 11. Department of Emergency Medicine and Surgery, Hôspital Pitié-Salpétrière, APHP, Université Pierre et Marie Curie-Paris 6 (UPMC), Paris, France. 12. Clinical Chemistry Laboratory, Groupe Hospitalier Cochin-Broca-Hôtel Dieu, Université Paris Descartes, Assistance Publique des Hôpitaux de Paris, Paris, France. 13. Cardiology Department, Groupe Hospitalier Cochin-Broca-Hôtel Dieu, Université Paris Descartes, Assistance Publique des Hôpitaux de Paris, Paris, France; Cardiology Department, Paris XIII University, Avicenne Hospital, Bobigny, France. 14. Department of Medical Sciences, Uppsala University, Uppsala, Sweden. 15. Department of Coronary and Structural Heart Diseases, National Insititute of Cardiology, Warsaw, Poland. 16. Division of Emergency Medicine, Stanford University School of Medicine, Stanford, CA. 17. Department of Laboratory Medicine, University of California, San Francisco, CA. 18. Servei de Bioquímica Clínica, Hospital de Sant Pau, Barcelona, Spain; Biochemistry and Molecular Biology Department, Universitat Autònoma, Barcelona, Spain. 19. Division of Cardiology, Mayo Clinic College of Medicine, Rochester, MN; Department of Laboratory Medicine and Pathology, Mayo Clinic College of Medicine, Rochester, MN. 20. Department of Cardiology, University Hospital Basel, Basel, Switzerland; Universitäres Herz-Zentrum Bad Krozingen, Bad Krozingen, Germany. 21. Department of Cardiology, University Hospital Basel, Basel, Switzerland. 22. MedStar Cardiovascular Research Network, MedStar Heart Institute, Medstar Washington Hospital Center, Washington, DC. Electronic address: ron.waksman@medstar.net.
Abstract
BACKGROUND: Multiple studies have evaluated the diagnostic and prognostic performance of conventional troponin (cTn) and high-sensitivity troponin (hs-cTn). We performed a collaborative meta-analysis comparing cTn and hs-cTn for diagnosis of acute myocardial infarction (AMI) and assessment of prognosis in patients with chest pain. METHODS: MEDLINE/PubMed, Cochrane CENTRAL, and EMBASE were searched for studies assessing both cTn and hs-cTn in patients with chest pain. Study authors were contacted and many provided previously unpublished data. RESULTS: From 17 included studies, there were 8,644 patients. Compared with baseline cTn, baseline hs-cTn had significantly greater sensitivity (0.884 vs 0.749, P < .001) and negative predictive value (NPV; 0.964 vs 0.935, P < .001), whereas specificity (0.816 vs 0.938, P < .001) and positive predictive value (0.558 vs 0.759, P < .001) were significantly reduced. Based on summary receiver operating characteristic curves, test performance for the diagnosis of AMI was not significantly different between baseline cTn and hs-cTn (0.90 [95% CI 0.85-0.95] vs 0.92 [95% CI 0.90-0.94]). In a subanalysis of 6 studies that alternatively defined AMI based on hs-cTn, cTn had lower sensitivity (0.666, P < .001) and NPV (0.906, P < .001). Elevation of baseline hs-cTn, but negative baseline cTn, was associated with increased risk of death or nonfatal myocardial infarction during follow-up (P < .001) compared with both negative. CONCLUSION: High-sensitivity troponin has significantly greater early sensitivity and NPV for the diagnosis of AMI at the cost of specificity and positive predictive value, which may enable early rule in/out of AMI in patients with chest pain. Baseline hs-cTn elevation in the setting of negative cTn is also associated with increased nonfatal myocardial infarction or death during follow-up.
BACKGROUND: Multiple studies have evaluated the diagnostic and prognostic performance of conventional troponin (cTn) and high-sensitivity troponin (hs-cTn). We performed a collaborative meta-analysis comparing cTn and hs-cTn for diagnosis of acute myocardial infarction (AMI) and assessment of prognosis in patients with chest pain. METHODS: MEDLINE/PubMed, Cochrane CENTRAL, and EMBASE were searched for studies assessing both cTn and hs-cTn in patients with chest pain. Study authors were contacted and many provided previously unpublished data. RESULTS: From 17 included studies, there were 8,644 patients. Compared with baseline cTn, baseline hs-cTn had significantly greater sensitivity (0.884 vs 0.749, P < .001) and negative predictive value (NPV; 0.964 vs 0.935, P < .001), whereas specificity (0.816 vs 0.938, P < .001) and positive predictive value (0.558 vs 0.759, P < .001) were significantly reduced. Based on summary receiver operating characteristic curves, test performance for the diagnosis of AMI was not significantly different between baseline cTn and hs-cTn (0.90 [95% CI 0.85-0.95] vs 0.92 [95% CI 0.90-0.94]). In a subanalysis of 6 studies that alternatively defined AMI based on hs-cTn, cTn had lower sensitivity (0.666, P < .001) and NPV (0.906, P < .001). Elevation of baseline hs-cTn, but negative baseline cTn, was associated with increased risk of death or nonfatal myocardial infarction during follow-up (P < .001) compared with both negative. CONCLUSION: High-sensitivity troponin has significantly greater early sensitivity and NPV for the diagnosis of AMI at the cost of specificity and positive predictive value, which may enable early rule in/out of AMI in patients with chest pain. Baseline hs-cTn elevation in the setting of negative cTn is also associated with increased nonfatal myocardial infarction or death during follow-up.
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