Objective: Cardiac troponin elevation has been shown to be associated with adverse outcomes after percutaneous coronary intervention (PCI) for various subgroups of coronary artery disease. We sought to determine the prognostic significance of cardiac troponin I (cTnI) in patients with non-ST-elevation acute coronary syndromes (NSTE-ACS) treated with PCI.
Methods: The study consisted of 760 consecutive patients undergoing PCI for NSTE-ACS. Levels of cTnI were obtained repeatedly every 6 h before PCI. Peak cTnI levels were used for analysis. Patients were followed for major adverse cardiac events (MACE) defined as death, myocardial infarction, and urgent target vessel revascularization for a mean follow-up of 2.9 years.
Results: Patients with normal cTnI levels (≤1.0 ng/ml) were classified into subgroup 1. The remaining patients were divided based on an optimal cut-off value derived from the receiver operating characteristic analysis into subgroups 2 (1.1–20 ng/ml) and 3 (>20 ng/ml). By multivariate analyses, patients with higher peak preprocedural cTnI levels were independently associated with increased risk of 30-day mortality [adjusted odds ratio, 1.88, 95% confidence interval (CI): 1.11–3.17, P=0.019] and composite MACE [group 1 vs. group 2 (adjusted hazard ratio 2.09, 95% CI: 1.35–3.23, P<0.001), group 1 vs. group 3 (adjusted hazard ratio 3.64, 95% CI: 2.39–5.56, P<0.001)].
Conclusion: Preprocedural cTnI level is a strong and independent predictor of 30-day mortality and long-term MACE after PCI in the setting of NSTE-ACS.
aDivision of Cardiology, Department of Internal Medicine, Howard University Hospital, Washington, DC
bDepartment of Internal Medicine, John H. Stroger, Jr. Hospital of Cook County
cDivision of Cardiology, Department of Internal Medicine, John H. Stroger, Jr. Hospital of Cook County, Chicago, Illinois, USA
Correspondence to Sirikarn Napan, MD, Division of Cardiology, Department of Internal Medicine, Howard University Hospital, 2041 Georgia Avenue NW, Suite 3J-17, Washington, DC 20060, USA
Tel: +1 202 664 0652; fax: +1 202 591 1641;
Received 31 January 2010 Revised 11 March 2010 Accepted 29 March 2010