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Circulation. 2004;110:2342-2348
Published online before print October 11, 2004, doi: 10.1161/01.CIR.0000145166.44942.E0
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(Circulation. 2004;110:2342-2348.)
© 2004 American Heart Association, Inc.


Coronary Heart Disease

Cystatin C

A Novel Predictor of Outcome in Suspected or Confirmed Non–ST-Elevation Acute Coronary Syndrome

Tomas Jernberg, MD, PhD; Bertil Lindahl, MD, PhD; Stefan James, MD, PhD; Anders Larsson, MD, PhD; Lars-Olof Hansson, MD, PhD; Lars Wallentin, MD, PhD

From the Department of Medical Sciences, Cardiology and Uppsala Clinical Research Center (T.J., B.L., S.J., L.W.), and Department of Medical Sciences, Clinical Chemistry, University Hospital (A.L., L.-O.H.), Uppsala, Sweden.

Correspondence to Tomas Jernberg, MD, PhD, Department of Medical Sciences, Cardiology, Uppsala Research Center, University Hospital, 751 85 Uppsala, Sweden. E-mail tomas.jernberg{at}medsci.uu.se

Received March 28, 2004; revision received June 15, 2004; accepted June 18, 2004.

Background— Patients with suspected or confirmed non–ST-elevation acute coronary syndrome (ACS) constitute a large and heterogeneous group. Measurements of renal function such as serum creatinine and estimation of creatinine clearance carry independent prognostic information in this population. Cystatin C is a new and better marker of renal function than creatinine. The aim was therefore to evaluate the prognostic value of cystatin C in this population.

Methods and Results— Cystatin C was analyzed on admission in 726 patients admitted because of symptoms suggestive of an acute coronary syndrome and no ST-segment elevations. Patients were followed up with regard to death and myocardial infarction for a median of 40 and 6 months, respectively. The median cystatin C level was 1.00 mg/L (25th to 75th percentile, 0.83 to 1.24 mg/L). The risk of death during follow-up increased with increasing levels of cystatin C. In the group with non–ST-elevation ACS, patients in the second, third, and fourth quartiles had a relative risk of subsequent death of 1.8 (95% CI, 0.6 to 5.3), 3.2 (95% CI, 1.2 to 8.5), and 11.7 (95% CI, 4.7 to 29.3) compared with the lowest quartile. In Cox regression models including well-known predictors of outcome, cystatin C level was independently associated with mortality but not with the risk of subsequent myocardial infarction. In a comparison of the markers of renal function in receiver-operating curve analyses, cystatin C had the best ability to discriminate between survivors and nonsurvivors.

Conclusions— A single measurement of cystatin C will substantially improve the early risk stratification of patients with suspected or confirmed non–ST-elevation ACS.


Key Words: angina • cystatins • kidney • myocardial infarction • prognosis




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