Display Settings:

Format

Send to:

Choose Destination
Am Heart J. 2004 Nov;148(5):776-82.

Prognostic value of low-level cardiac troponin-I elevations in patients without definite acute coronary syndromes.

Author information

  • 1General Internal Medicine Section, Veterans Affairs Medical Center, and the Division of General Internal Medicine, Department of Medicine, University of California San Francisco, San Francisco, Calif, USA. mpham@stanford.edu

Abstract

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.

Comment in

PMID:
15523306
[PubMed - indexed for MEDLINE]
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk