The prognostic and therapeutic implications of increased troponin T levels and ST depression in unstable coronary artery disease: The FRISC II invasive troponin T electrocardiogram substudy☆☆☆★
Abstract
Background In unstable coronary artery disease, both increased troponin T level and occurrence of ST-segment depression are associated with a worse prognosis. In the Fast Revascularisation in InStability in Coronary disease trial II invasive study, we evaluated whether the troponin T level, alone and combined with ST depression, identified more severe coronary artery disease or a greater efficacy of an early invasive strategy. Methods In the study, 2457 patients with unstable coronary artery disease were randomized to early invasive or noninvasive strategy. Troponin T value and admission electrocardiogram results were available in 2286 patients. Results In the noninvasive cohort, death or myocardial infarction occurred in 16.6% with troponin T level ≥0.03 μg/L versus 8.5% with troponin T level <0.03 μg/L (P < .001). In the invasive group, 49% of patients with both ST depression and troponin T level ≥0.03 μg/L had 3-vessel or left main disease compared with 17% if neither finding was present (P < .001). The invasive strategy reduced death/myocardial infarction at 12 months in the cohort with both ST depression and troponin T level ≥0.03 μg/L from 22.1% to 13.2% (risk ratio, 0.60; 95% confidence interval, 0.43 to 0.82; P = .001). In the cohort with either ST depression or troponin T level ≥0.03 μg/L or neither of these findings, the absolute gain of the invasive strategy was smaller and more uncertain. Conclusion Patients with unstable coronary artery disease with the combination of troponin T level ≥0.03 μg/L and ST depression have a poor prognosis and, in half of the cases, 3-vessel or left main disease. In these patients, an early invasive strategy will substantially reduce death/myocardial infarction. (Am Heart J 2002;143:760-7.)
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☆ Supported by and organized in collaboration with the Pharmacia & Upjohn Company. Project organization within the research group also supported by the Swedish Heart-Lung Foundation and Uppsala County Association Against Heart and Lung Diseases.
☆☆ Reprint requests: Erik Diderholm, MD, Department of Cardiology, Cardiothoracic Center, University Hospital, S-751 85 Uppsala, Sweden.
★ E-mail: erik.diderholm@card.uas.lul.se
PII: S0002-8703(02)84211-9
doi:10.1067/mhj.2002.121733
© 2002 Mosby, Inc. All rights reserved.
