Prognostic value of low-level cardiac troponin-I elevations in patients without definite acute coronary syndromes - 26/08/11
, Mary A. Whooley, MD a, G.Thomas Evans, MD b, †, Catherine Liu, MD a, Homeira Emadi, MD a, Winnie Tong, MD a, M.Catherine Murphy, MD a, Kirsten E. Fleischmann, MD, MPH, FACC bAbstract |
Background |
Low-level cardiac troponin-I (cTn-I) elevations predict adverse cardiovascular outcomes in patients with definite acute coronary syndromes (ACS), as defined by the presence of chest pain accompanied by ischemic electrocardiographic changes. However, their prognostic value in other clinical situations remains unclear.
Methods |
We studied 366 patients with suspected myocardial infarction (MI) but without definite ACS, including 57 patients with low-level cTn-I elevations (1.0 to 3.0 ng/mL) and 309 patients with cTn-I <1.0 ng/mL. All cTn-I measurements were made with the Dade Stratus II analyzer. We determined the adjusted 1-year risk of nonfatal MI or death from coronary heart disease (CHD death) in each group by using Cox proportional hazards models.
Results |
Among patients with cTn-I elevations between 1.0 and 3.0 ng/mL, 6 (11%) had a nonfatal MI or CHD death at 1 year compared with 12 (4%) patients in the cTn-I <1.0 ng/mL group [hazard ratio (HR), 3.5; 95% CI, 1.4 to 8.8]. After adjusting for baseline clinical characteristics, cTn-I levels between 1.0 and 3.0 ng/mL remained strongly associated with nonfatal MI or CHD death (adjusted HR, 3.4; 95% CI, 1.3 to 9.4). This association persisted even in the 215 patients who presented without chest pain (adjusted HR, 4.3; 95% CI, 1.4 to 13).
Conclusions |
Low-level cTn-I elevations identify a subset of patients at increased risk for future cardiovascular events, even when obtained outside the context of definite ACS or presentation with chest pain.
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 | Dr Whooley is supported by the Department of Veterans Affairs Health Services Research and Development Service (Advanced Research Career Development Award), the Robert Wood Johnson Foundation (Generalist Physician Faculty Scholars Program), and the American Federation for Aging Research (Paul Beeson Faculty Scholars in Aging Research Program). |
Vol 148 - N° 5
P. 776-782 - novembre 2004 Retour au numéro
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