Elevated troponin T on discharge predicts poor outcome of decompensated heart failure

Kimi Koide1, Tsutomu Yoshikawa, Yuji Nagatomo

  • 1Cardiology Division, Department of Medicine, Keio University School of Medicine, 35 Shinanomachi, Shinjuku-ku, Tokyo 160-8582, Japan.

Heart and Vessels
|June 1, 2010
PubMed

Insights

Persistent elevation of cardiac troponin T (cTnT) in heart failure (HF) patients predicts worse outcomes. This elevation is linked to inflammation, higher brain natriuretic peptide (BNP) levels, diabetes, and anemia, and is reduced by beta-blocker therapy.

Area of Science:

  • Cardiology
  • Biomarkers
  • Heart Failure Pathophysiology

Background:

  • Persistent elevation of cardiac troponin T (cTnT) is linked to poor prognosis in chronic heart failure (HF).
  • The mechanisms connecting predischarge cTnT levels to underlying pathophysiology in decompensated HF require further investigation.

Purpose of the Study:

  • To explore the association between elevated predischarge cTnT levels and specific pathophysiological factors in patients hospitalized for decompensated HF.
  • To determine if predischarge cTnT elevation independently predicts adverse clinical outcomes after hospital discharge.

Main Methods:

  • A cohort of 170 patients with decompensated HF had plasma cTnT levels measured before discharge.
  • Patients were stratified into cTnT-positive (n=40) and cTnT-negative (n=130) groups.
  • Multivariate and Cox proportional hazards analyses were used to identify predictors of cTnT positivity and mortality.

Main Results:

  • Predischarge cTnT elevation was independently associated with lack of beta-blocker use, elevated high-sensitivity C-reactive protein (hsCRP), high brain natriuretic peptide (BNP), diabetes, and anemia.
  • The cTnT-positive group experienced significantly higher rates of total mortality, cardiac death, and HF exacerbations requiring hospitalization.
  • cTnT positivity was an independent predictor of mortality (HR=5.008, P=0.004) in a matched model.

Conclusions:

  • Elevated predischarge cTnT in decompensated HF patients reflects significant underlying pathophysiology, including inflammation and neurohormonal activation.
  • cTnT elevation identifies patients at high risk for adverse outcomes, including mortality and rehospitalization.
  • Optimizing medical therapy, such as beta-blocker use, and managing comorbidities like diabetes and anemia may be crucial in patients with elevated cTnT.

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