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Technical Briefs |
1 Hennepin County Medical Center and University of Minnesota School of Medicine, Department of Laboratory Medicine and Pathology, Minneapolis, MN 55415
2 Medical College of Virginia, Department of Medicine, Richmond, VA 23225
3 Alameda County Medical CenterHighland Campus, Department of Emergency Medicine, Oakland, CA 94602
4 University of Minnesota School of Medicine, Divisions of Cardiology and Epidemiology, Minneapolis, MN 55454
5 Statistical Consulting, Minot, ND 58703
6 St. Georges Hospital, Clinical Biochemistry Department, London SW17 0QT, United Kingdom
aaddress correspondence to this author at: Hennepin County Medical Center, Clinical Laboratories MC 812, 701 Park Ave., Minneapolis, MN 55415; fax 612-904-4229, e-mail fred.apple@co.hennepin.mn.us
| The first 300 words of the full text of this article appear below. |
Numerous studies have evaluated cardiac troponin I (cTnI), cardiac troponin T (cTnT), and creatine kinase-MB for risk stratification of acute coronary syndrome (ACS) patients. Two metaanalyses have demonstrated the ability of cTnI or cTnT to predict adverse outcomes (1)(2). A substudy of the FRISC II trial showed that the prognostic value of cTnT in ACS patients could be attributed to its correlation with the underlying severity of coronary artery stenosis (3).
Because of analytical and clinical differences among troponin assays (4)(5)(6)(7), the cardiology (8)(9) and laboratory medicine (10) communities have endorsed the need for evidence-based studies before individual assays are accepted into clinical practice. Few studies have investigated the role of point-of-care (POC) testing for assessing adverse outcomes in ACS patients. One study using qualitative POC assays for cTnI and cTnT showed both assays to be independent predictors of cardiac events at 30 days after admission in ACS patients (11).
In a consensus document from the European Society of Cardiology (ESC) and the American College of Cardiology (ACC), myocardial infarction (MI) was redefined as any amount of myocardial necrosis in the presence of myocardial ischemia, as indicated by an increased cardiac troponin (I or T) above the 99th percentile of a reference population (9). Because many troponin assays lack acceptable precision at the 99th percentile cutoff and assay precision may be important for risk stratification, a revised cutoff has been recommended as the index for myocardial damage, as the lowest troponin concentration closest to the 99th percentile that can be measured with 10% imprecision (CV) (5).
We investigated the prognostic value of a whole-blood quantitative POC cTnI assay for risk stratification of ACS patients
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