Minor myocardial damage detected by troponin T is a powerful predictor of long-term prognosis in patients with acute decompensated heart failure.

BACKGROUND: The progression of chronic heart failure (CHF) is characterized by frequent exacerbation requiring hospitalization and high mortality. Clinical deterioration is triggered by many factors that could promote ongoing myocytes injury. We sought to determine whether a specific marker of cardiac injury, troponin T (cTnT), is associated with prognosis in acute decompensated heart failure (ADHF). METHODS: One hundred and eighty-four consecutive patients with ADHF were enrolled in the absence of an acute coronary syndrome. A cTnT value> or =0.1 ng/ml in samples drawn at 6, 12 or 24 h after hospital admission was considered abnormal. RESULTS: Increased levels of cTnT were found in 58 patients (31.5%, group 1). There were no significant differences between group 1 and patients with cTnT<0.1 ng/ml (group 2) in terms of demographic and clinical characteristics, although ischemic etiology was more prevalent in group 1 (51.7% vs. 31.7%, p=0.009). During follow-up, the mortality in groups 1 and 2 was 31% and 17.5% (p=0.038, OR=2.13, 95% CI: 1.03-4.69), respectively. The 3-year free-CHF readmission survival in group 1 and 2 was 25% and 53% (log rank test p=0.015). In a Cox proportional hazard model, poor tissue perfusion (HR=2.46, 95% CI=1.31-4.6), previous infarction (HR=1.99, 95% CI=1.02-3.9) and cTnT> or =0.1 ng/ml (HR=1.74, 95% CI=1.05-2.9) emerged as the independent predictors of long-term outcome. CONCLUSIONS: One third of patients with decompensated CHF had elevated levels of cTnT. Troponin T was an independent long-term prognostic marker of morbidity and mortality and it suggests a role of biochemical risk stratification in this setting.

High levels of troponin T are associated with ventricular remodeling and adverse in-hospital outcome in heart failure.

BACKGROUND: Heart failure progression is associated with ventricular remodeling and ongoing myofibrillar degradation. We hypothesized that myocardial damage, detected by high levels of troponin T, would correlate with echocardiographic measurements of left ventricular remodeling and worse in-hospital course in decompensated heart failure. MATERIAL/METHODS: 159 patients with decompensated heart failure without acute coronary event were included. A troponin T value >0.2 ng/ml in samples taken 6, 12 or 24 hours after admission was considered abnormal. RESULTS: High troponin T levels were identified in 24 patients (15%) (Group 1). Mean age for group 1 was 65.9 vs. 63.7 years in patients with troponin T<0.2 (Group 2) (p=ns). Ischemic etiology in groups 1 and 2 was found in 58.3 and 38.5% (p=0.07). Two-dimensional echocardiograms in groups 1 and 2 revealed higher left ventricular diameters, diastolic (61.7+/-10 vs. 56.9+/-10.3 mm, p=0.041) as well as systolic (49.4+/-13.5 vs. 42.0+/-12.0 mm, p=0.012), and lower ejection fraction (30.1+/-14 vs. 39.0+/-17.7%, p=0.03). Incidence of combined end point of death or refractory heart failure was 20.8 and 3.7% in groups 1 and 2 (p=0.007; OR=6.8; CI95%=1.5-31.2). In a multiple regression model, a history of infarction and chronic obstructive pulmonary disease, tissue hypoperfusion, radiographic pulmonary edema, and high troponin T levels emerged as the independent predictors. CONCLUSIONS: High troponin T levels were found in 15% of patients with acute exacerbation of heart failure; this finding was independently associated with worse prognosis. Echocardiograms suggested that more severe ventricular remodeling is one subjacent mechanism related with biochemically detected myocardial injury in this setting.