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Received on July 20, 2006
Accepted on November 30, 2006
Evidence-Based Laboratory Medicine and Test Utilization |
1 Department of Pathology and Molecular Medicine, McMaster University, Hamilton, ON, Canada
2 Institute for Clinical Evaluative Sciences, University of Toronto, Toronto, ON, Canada
3 Department of Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, ON, Canada
4 Department of Pathology, Women and Infants Hospital, Providence, RI
5 Cardiovascular Division and Division of Laboratory Medicine, Mayo Clinic, Rochester, MN
* To whom correspondence should be addressed. E-mail: kavsakp{at}mcmaster.ca.
Background: Recent data suggest that older men with detectable cardiac troponin I (cTnI) concentrations that remain below the 99th percentile concentration cutoff are at increased risk for subsequent cardiovascular events. We designed this study to extend this observation by examining risk prediction in both men and women presenting to an emergency department with chest discomfort.
Methods: We obtained data for all-cause mortality and hospital discharges associated with either acute myocardial infarction (AMI) or congestive heart failure (CHF) for up to 8 years after the initial presentation in 448 patients who originally presented in 1996 with acute coronary syndrome (ACS). We performed retrospective analysis for cTnI (AccuTnITM; Beckman Coulter) in frozen plasma samples based on the patients' reported time from onset of symptoms. Peak cTnI concentration was used for risk assessment.
Results: Patients with cTnI concentrations 
0.02 µg/L (i.e., limit of detection), including those whose peak values remained below the 99th percentile (0.04 µg/L), were at greater risk for death and AMI/CHF readmissions at 2, 5, and 8 years of follow-up compared with those with peak cTnI <0.02 µg/L. All results were statistically significant (P <0.05) except for death within 2 years among patients with normal but detectable cTnI (0.02 to 0.03 µg/L), relative to the group with values <0.02 µg/L. Kaplan-Meier analyses indicated that both men and women with cTnI 0.02 µg/L had worse outcomes (P <0.001).
Conclusion: Both men and women who present with possible ACS with detectable cTnI concentrations that remain below the 99th percentile are at a greater risk for future adverse events.
The following articles in journals at HighWire Press have cited this article:
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  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]
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 P. Venge, N. Johnston, B. Lindahl, and S. James Normal plasma levels of cardiac troponin I measured by the high-sensitivity cardiac troponin I access prototype assay and the impact on the diagnosis of myocardial ischemia. J. Am. Coll. Cardiol., September 22, 2009; 54(13): 1165 - 1172. [Abstract] [Full Text] [PDF]
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P. A. Kavsak, A. R. MacRae, M.-J. Yerna, and A. S. Jaffe Analytic and Clinical Utility of a Next-Generation, Highly Sensitive Cardiac Troponin I Assay for Early Detection of Myocardial Injury Clin. Chem., March 1, 2009; 55(3): 573 - 577. [Abstract] [Full Text] [PDF]
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 H.A. Katus, E. Giannitsis, A.S. Jaffe, and K. Thygesen Higher sensitivity troponin assays: Quo vadis? Eur. Heart J., January 2, 2009; 30(2): 127 - 128. [Full Text] [PDF]
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A. H.B. Wu, Q. A. Lu, J. Todd, J. Moecks, and F. Wians Short- and Long-Term Biological Variation in Cardiac Troponin I Measured with a High-Sensitivity Assay: Implications for Clinical Practice Clin. Chem., January 1, 2009; 55(1): 52 - 58. [Abstract] [Full Text] [PDF]
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P. Venge, S. James, L. Jansson, and B. Lindahl Clinical Performance of Two Highly Sensitive Cardiac Troponin I Assays Clin. Chem., January 1, 2009; 55(1): 109 - 116. [Abstract] [Full Text] [PDF]
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K. Kurz, E. Giannitsis, J. Zehelein, and H. A. Katus Highly Sensitive Cardiac Troponin T Values Remain Constant after Brief Exercise- or Pharmacologic-Induced Reversible Myocardial Ischemia Clin. Chem., July 1, 2008; 54(7): 1234 - 1238. [Abstract] [Full Text] [PDF]
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P. A. Kavsak, A. M. Newman, D. T. Ko, G. E. Palomaki, V. Lustig, A. R. MacRae, and A. S. Jaffe Is a Pattern of Increasing Biomarker Concentrations Important for Long-Term Risk Stratification in Acute Coronary Syndrome Patients Presenting Early after the Onset of Symptoms? Clin. Chem., April 1, 2008; 54(4): 747 - 751. [Abstract] [Full Text] [PDF]
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P. A. Kavsak, D. T. Ko, A. M. Newman, G. E. Palomaki, V. Lustig, A. R. MacRae, and A. S. Jaffe Risk Stratification for Heart Failure and Death in an Acute Coronary Syndrome Population Using Inflammatory Cytokines and N-Terminal Pro-Brain Natriuretic Peptide Clin. Chem., December 1, 2007; 53(12): 2112 - 2118. [Abstract] [Full Text] [PDF]
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 K. M. Eggers, B. Lagerqvist, P. Venge, L. Wallentin, and B. Lindahl Persistent Cardiac Troponin I Elevation in Stabilized Patients After an Episode of Acute Coronary Syndrome Predicts Long-Term Mortality Circulation, October 23, 2007; 116(17): 1907 - 1914. [Abstract] [Full Text] [PDF]
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