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Previous Volume 358:2117-2126 May 15, 2008 Number 20 Next

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ABSTRACT

Background Cardiac troponin provides diagnostic and prognostic information in acute coronary syndromes, but its role in acute decompensated heart failure is unclear. The purpose of our study was to describe the association between elevated cardiac troponin levels and adverse events in hospitalized patients with acute decompensated heart failure.

Methods We analyzed hospitalizations for acute decompensated heart failure between October 2001 and January 2004 that were recorded in the Acute Decompensated Heart Failure National Registry (ADHERE). Entry criteria included a troponin level that was obtained at the time of hospitalization in patients with a serum creatinine level of less than 2.0 mg per deciliter (177 µmol per liter). A positive troponin test was defined as a cardiac troponin I level of 1.0 µg per liter or higher or a cardiac troponin T level of 0.1 µg per liter or higher.

Results Troponin was measured at the time of admission in 84,872 of 105,388 patients (80.5%) who were hospitalized for acute decompensated heart failure. Of these patients, 67,924 had a creatinine level of less than 2.0 mg per deciliter. Cardiac troponin I was measured in 61,379 patients, and cardiac troponin T in 7880 patients (both proteins were measured in 1335 patients). Overall, 4240 patients (6.2%) were positive for troponin. Patients who were positive for troponin had lower systolic blood pressure on admission, a lower ejection fraction, and higher in-hospital mortality (8.0% vs. 2.7%, P<0.001) than those who were negative for troponin. The adjusted odds ratio for death in the group of patients with a positive troponin test was 2.55 (95% confidence interval, 2.24 to 2.89; P<0.001 by the Wald test).

Conclusions In patients with acute decompensated heart failure, a positive cardiac troponin test is associated with higher in-hospital mortality, independently of other predictive variables. (ClinicalTrials.gov number, NCT00366639 [ClinicalTrials.gov] .)

Source Information

From the Department of Emergency Medicine, Cleveland Clinic Foundation, Cleveland (W.F.P.); the Division of Cardiology (T.D.M.) and the Department of Laboratory Medicine (A.H.B.W.), University of California at San Francisco, San Francisco; Ahmanson–UCLA Cardiomyopathy Center, UCLA, Los Angeles (G.C.F.); the Department of Emergency Medicine, University of California, Davis, Sacramento (D.D.); the Department of Statistics, Scios, Mountain View, CA (J.W.); and the Department of Laboratory Medicine and Pathology, Hennepin County Medical Center and University of Minnesota School of Medicine, Minneapolis (F.S.A.).

Address reprint requests to Dr. Peacock at the Department of Emergency Medicine E19, Cleveland Clinic Foundation, 9500 Euclid Ave., Cleveland OH 44195, or at peacocw{at}ccf.org.

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