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.
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.
Abstract:
Persistent elevation of cardiac troponin T (cTnT) predicts an adverse clinical outcome in patients with chronic heart failure (HF), but the underlying mechanisms remain to be determined. We investigated the association between predischarge cTnT elevation and coexistent pathophysiology in patients with decompensated HF. Plasma cTnT levels were determined before discharge in 170 patients with decompensated HF. We divided the patients into a group that was positive for cTnT [cTnT(+) group, n = 40] and a group that was negative for cTnT [cTnT(-) group, n = 130]. Multivariate analysis showed that use of beta-blocker therapy (odds ratio [OR] = 0.236, P = 0.003), an elevated high-sensitivity C-reactive protein (hsCRP) level (OR = 3.731, P = 0.006), a high brain natriuretic peptide (BNP) level (OR = 3.570, P = 0.007), diabetes (OR = 3.090, P = 0.018), and anemia (OR = 2.330, P = 0.047) were independently associated with cTnT positivity. During a mean follow-up period of 441 days after discharge, total mortality (P < 0.001), cardiac death (P < 0.001), and exacerbation of HF requiring hospitalization (P = 0.007) were all more common in the cTnT(+) group than in the cTnT(-) group. Cox proportional hazards analysis showed that cTnT positivity was an independent predictor of total mortality (hazard ratio = 5.008, P = 0.004) in an age- and gender-matched model. Elevation of cTnT during convalescence was associated with lack of beta-blocker therapy, a high hsCRP level at discharge, a high BNP level at discharge, diabetes, and anemia, and a worse clinical outcome in patients with decompensated HF.
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