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 β-blocker therapy (odds ratio [OR] = 0.236, P = 0.003), an elevated highsensitivity 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 β-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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