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Background Cardiac troponin testing is central to the diagnosis of acute myocardial infarction. We evaluated a sensitive troponin I assay for the early diagnosis and risk stratification of myocardial infarction.
Methods In a multicenter study, we determined levels of troponin I as assessed by a sensitive assay, troponin T, and traditional myocardial necrosis markers in 1818 consecutive patients with suspected acute myocardial infarction, on admission and 3 hours and 6 hours after admission.
Results For samples obtained on admission, the diagnostic accuracy was highest with the sensitive troponin I assay (area under the receiver-operating-characteristic curve [AUC], 0.96), as compared with the troponin T assay (AUC, 0.85) and traditional myocardial necrosis markers. With the use of the sensitive troponin I assay (cutoff value, 0.04 ng per milliliter) on admission, the clinical sensitivity was 90.7%, and the specificity was 90.2%. The diagnostic accuracy was virtually identical in baseline and serial samples, regardless of the time of chest-pain onset. In patients presenting within 3 hours after chest-pain onset, a single sensitive troponin I assay had a negative predictive value of 84.1% and a positive predictive value of 86.7%; these findings predicted a 30% rise in the troponin I level within 6 hours. A troponin I level of more than 0.04 ng per milliliter was independently associated with an increased risk of an adverse outcome at 30 days (hazard ratio, 1.96; 95% confidence interval, 1.27 to 3.05; P=0.003).
Conclusions The use of a sensitive assay for troponin I improves early diagnosis of acute myocardial infarction and risk stratification, regardless of the time of chest-pain onset.
Source Information
From the Department of Medicine II (T.K., T.Z., S.T., A.R., E.C., A.W., C.R.S., M.S.E., P.S.W., R.B.S., E.L., S.G.-Z., F.P., T.F.M., S.B.) and the Institute for Clinical Chemistry and Laboratory Medicine (D.P., N.J., K.J.L.), University Medical Center, Johannes Gutenberg University, Mainz; the Department of Internal Medicine, Federal Armed Forces Hospital, Koblenz (C.B.); and the Department of Cardiology and Angiology, Heart Center, University Hospital Hamburg-Eppendorf, Hamburg (S.B., M.F.) — all in Germany; Boston University School of Medicine, the Framingham Heart Study, Framingham, MA (R.B.S.); the Department of Medicine, Brigham and Women's Hospital, and Harvard Medical School — both in Boston (E.L.); and INSERM Unité 525, Faculté de Médecine Pitié–Salpêtrière, Paris (V.N., L.T.).
Drs. Keller, Zeller, and Peetz contributed equally to this article.
Address reprint requests to Dr. Blankenberg at Langenbeckstr. 1, 55101 Mainz, Germany, or at blankenberg{at}2-med.klinik.uni-mainz.de.
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