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Published at www.nejm.org November 25, 2009 (10.1056/NEJMoa0805299)

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ABSTRACT

Background In most patients with stable coronary artery disease, plasma cardiac troponin T levels are below the limit of detection for the conventional assay. The distribution and determinants of very low circulating troponin T levels, as well as their association with cardiovascular events, in such patients are unknown.

Methods We used a new, high-sensitivity assay to determine the concentration of cardiac troponin T in plasma samples from 3679 patients with stable coronary artery disease and preserved left ventricular function. Results of the assay were analyzed in relation to the incidence of cardiovascular events during a median follow-up period of 5.2 years.

Results With the highly sensitive assay, concentrations of cardiac troponin T were at or above the limit of detection (0.001 µg per liter) in 3593 patients (97.7%) and at or above the 99th percentile for apparently healthy subjects (0.0133 µg per liter) in 407 patients (11.1%). After adjustment for other independent prognostic indicators, there was a strong and graded increase in the cumulative incidence of cardiovascular death (adjusted hazard ratio per unit increase in the natural logarithm of the troponin T level, 2.09; 95% confidence interval [CI], 1.60 to 2.74; P<0.001) and of heart failure (adjusted hazard ratio, 2.20; 95% CI, 1.66 to 2.90; P<0.001) in this study group. Increased risk associated with higher levels of troponin T was evident well below the limit of detection of conventional cardiac troponin T assays and below the 99th percentile of values in a healthy population. There was no association between troponin T levels as measured with the highly sensitive assay and the incidence of myocardial infarction (adjusted hazard ratio, 1.16; 95% CI, 0.97 to 1.40; P=0.11).

Conclusions After adjustment for other independent prognostic indicators, cardiac troponin T concentrations as measured with a highly sensitive assay were significantly associated with the incidence of cardiovascular death and heart failure but not with myocardial infarction in patients with stable coronary artery disease.

Source Information

From the Division of Medicine (T.O.) and the Center of Laboratory Medicine (S.T.), Akershus University Hospital, Lørenskog, Norway; the Faculty Division Akershus University Hospital and the Center for Heart Failure Research, University of Oslo, Oslo (T.O.); the Department of Medicine, University of Texas Southwestern Medical Center, Dallas (J.A.L.); the Department of Medicine, Harvard Medical School, and the Cardiovascular Division, Brigham and Women's Hospital — both in Boston (M.S.S., M.A.P., E.B.); the Biostatistics Center, George Washington University, Rockville, MD (C.A.C., M.M.R., K.A.J.); National Heart, Lung, and Blood Institute, Bethesda, MD (M.J.D.); the Division of Cardiovascular Diseases, Department of Medicine, Mayo Clinic, Rochester, MN (B.J.G.); and Montreal Heart Institute, and Faculty of Medicine, University of Montreal — both in Montreal (J.L.R.).

This article (10.1056/NEJMoa0805299) was published on November 25, 2009, at NEJM.org.

Address reprint requests to Dr. Omland at the Division of Medicine, Akershus University Hospital, NO-1478 Lørenskog, Norway, or at torbjorn.omland{at}medisin.uio.no.

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