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.