| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Editorials |
TIMI Study Group, Cardiovascular Division, Department of Medicine, Brigham & Women’s Hospital, Boston, MA
aAddress correspondence to this author at:, Cardiovascular Division, Brigham and Women’s Hospital, 75 Francis St., Boston, MA 02115, Fax 617-734-7139, E-mail dmorrow@partners.org
| The first 300 words of the full text of this article appear below. |
Despite the facts that cardiac troponin was introduced 2 decades ago and has been established since 2000 as the preferred biomarker for the diagnosis of myocardial infarction (MI)1 (1), the clinical application of cardiac troponin assays continues to evolve substantively. In large part, this evolution has been driven by sustained progress in the analytical performance of commercially available cardiac troponin assays. Because of improved precision at low cardiac troponin concentrations and data establishing the prognostic relevance of quantitatively minor increases in this biomarker, the clinical decision limit for cardiac troponin has been pushed progressively lower. A recently emerged new generation of research assays for cardiac troponin now has reduced the limit of detection by another 10- to 100-fold compared with current commercially available assays (2)(3). In this issue of Clinical Chemistry, the report by Eggers et al. (4) and 2 reports by Wu et al. (5)(6) provide valuable insights into possible new applications for more sensitive assays, as well as raise new questions that must be addressed in the course of evaluation of a new generation of high-sensitivity cardiac troponin assays.
Where Are We Now?
Because cardiac troponin is superior to the previous gold standard (creatine kinase isoenzyme MB) for MI diagnosis, the initial efforts to establish a uniform diagnostic decision limit were difficult and at times controversial. This challenge was (and still is) compounded by a lack of standardization of the multiple commercial assays for cardiac troponin I (cTnI) and the poor precision of some assays around the proposed diagnostic cutoffs; however, the uncertainty regarding the clinical significance of increases in cardiac troponin that are below the concentration equivalent to an abnormal increase in creatine kinase MB has been resolved by consistent epidemiologic data that have established a relationship between
Where Are We Going?
Challenges Ahead
The following articles in journals at HighWire Press have cited this article:
|
|
 |
|
  P. A. Kavsak, X. Wang, D. T. Ko, A. R. MacRae, and A. S. Jaffe Short- and Long-Term Risk Stratification Using a Next-Generation, High-Sensitivity Research Cardiac Troponin I (hs-cTnI) Assay in an Emergency Department Chest Pain Population Clin. Chem., October 1, 2009; 55(10): 1809 - 1815. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 T. Keller, T. Zeller, D. Peetz, S. Tzikas, A. Roth, E. Czyz, C. Bickel, S. Baldus, A. Warnholtz, M. Frohlich, et al. Sensitive Troponin I Assay in Early Diagnosis of Acute Myocardial Infarction N. Engl. J. Med., August 27, 2009; 361(9): 868 - 877. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Emdin, S. Vittorini, C. Passino, and A. Clerico Old and new biomarkers of heart failure Eur J Heart Fail, April 1, 2009; 11(4): 331 - 335. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
