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Volume 45, Issue 4, Pages 355-362 (April 2005)


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Influence of Timing of Troponin Elevation on Clinical Outcomes and Use of Evidence-Based Therapies for Patients With Non–ST-Segment Elevation Acute Coronary Syndromes

For the CRUSADE InvestigatorsMatthew T. Roe, MD, MHSCorresponding Author Informationemail address, Eric D. Peterson, MD, MPH, Charles V. Pollack Jr., MA, MD, L. Kristin Newby, MD, MHS, Yun Li, MS, Robert H. Christenson, PhD, W. Frank Peacock, MD, Francis M. Fesmire, MD, Deborah Diercks, MD, J. Douglas Kirk, MD, Sidney C. Smith Jr., MD, E. Magnus Ohman, MD, W. Brian Gibler, MD

Received 18 August 2004; received in revised form 8 October 2004; accepted 12 October 2004. published online 07 February 2005.

Study objective

Previous studies in clinical trial populations have demonstrated that patients presenting with positive troponin levels have a higher risk of mortality than patients with later positive troponin levels, but the influence of the timing of troponin elevation has not been previously characterized. We evaluate the impact of the timing of troponin elevation on clinical outcomes and adherence to the American College of Cardiology/American Heart Association acute care guidelines for patients with non–ST-segment elevation acute coronary syndromes.

Methods

We examined inhospital outcomes and use of acute (<24 hours) medications and invasive cardiac procedures in 23,184 high-risk patients with non–ST-segment elevation acute coronary syndromes (positive cardiac markers or ischemic ST-segment changes) during 2001 to 2002 from 396 US hospitals participating in the Can Rapid Risk Stratification of Unstable Angina Patients Suppress ADverse Outcomes with Early Implementation of the American College of Cardiology/American Heart Association Guidelines (CRUSADE) Initiative. Baseline and peak troponin values were recorded and were designated as positive if above the cutoff value used at each institution to designate definite myocardial necrosis.

Results

In the study cohort, 53.2% of patients presented with baseline positive troponin levels, 30.6% had baseline negative/later positive troponin levels, and 16.2% had negative troponin levels during the entire hospitalization. Patients with baseline positive troponin levels had a higher risk of inhospital mortality than patients with baseline negative/later positive troponin levels (6.5% versus 4.1%) and were less likely to undergo early cardiac catheterization or percutaneous coronary intervention. The use of acute aspirin (in approximately 91% of patients), heparin (85%), and β-blockers (78%) was similar in patients with baseline-positive versus later-positive troponin levels.

Conclusion

These findings demonstrate that evidence-based therapies and interventions for non–ST-segment elevation acute coronary syndromes are underused in patients with elevated troponin levels, but baseline troponin elevations, which are associated with a higher risk of inhospital mortality, do not stimulate more aggressive care.

From the Duke Clinical Research Institute, Durham, NC (Roe, Peterson, Newby, Li); Pennsylvania Hospital, Philadelphia, PA (Pollack); University of Maryland School of Medicine, Baltimore, MD (Christenson); Cleveland Clinic Foundation, Cleveland, OH (Peacock); Erlanger Medical Center, Chattanooga, TN (Fesmire); University of California–Davis, Sacramento, CA (Diercks, Kirk); University of Cincinnati College of Medicine, Cincinnati, OH (Gibler); and University of North Carolina School of Medicine, Chapel Hill, NC (Smith, Ohman)

Corresponding Author InformationAddress for correspondence: Matthew T. Roe, MD, MHS, Duke Clinical Research Institute, 2400 Pratt Street, Durham, NC 27705; 919-668-8959, fax 919-668-7059

 Author contributions: MTR, EDP, WBG, and EMO conceived the study, designed the study, and obtained research funding. MTR, EDP, and LKN supervised the conduct of the study and data collection. CVP, RHC, WFP, FMF, DD, JDK, and SCS provided input into the study design, interpretation of the data, and writing of the manuscript. YL provided statistical advice on study design and analyzed the data. MTR drafted the manuscript, and all authors contributed substantially to its revision. MTR takes responsibility for the paper as a whole.

Funding and support: CRUSADE is funded by Millennium Pharmaceuticals, Inc., and Schering Corporation. Bristol-Myers Squibb/Sanofi Pharmaceuticals Partnership provides an unrestricted grant in support of the program.

Reprints not available from the authors.

PII: S0196-0644(04)01555-0

doi:10.1016/j.annemergmed.2004.10.016


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