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Eduardo Roque Perna, Stella Maris Macin, Juan Pablo Cimbaro Canella, Pablo Marcelo Alvarenga, Rolando Esteban Pantich, Nelson Gerardo Rios, Jorge Raúl Cialzeta, Eduardo Francisco Farias, Jorge Reynaldo Badaracco, Monica Brizuela, Eloisa Jantus, Emil D. Missov
Med Sci Monit 2004; 10(3): CR90-95
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.