BACKGROUND: Cardiac cell death has been shown to occur in heart failure and has been implicated as one of the mechanisms responsible for progression of the disease. Cardiac Troponin I (cTnI) represents a highly sensitive marker for myocardial cell death. Based on previous studies reporting that cTnI may be detected in patients with heart failure, we evaluated the clinical correlates and prognostic implications of detectable cTnI in a consecutive series of patients with severe heart failure. METHODS: Thirty-four patients were examined. Upon admission, we measured serum levels of cTnI by conventional immunoenzymatic assay (Stratus Dade II). According to the results of this assay, patients were divided into 2 groups, based on the presence (cTnI+) or absence (cTnI-) of detectable cTnI. These 2 groups were compared by non-parametric analysis for their clinical characteristics, instrumental findings, and short-term outcome. RESULTS: The cTnI+ group included 10 patients (29%) with a mean serum cTnI of 0.7 +/- 0.3 ng/ml. Compared with the cTnI- group, these patients had significantly lower left ventricular ejection fractions (20% +/- 5% vs 26% +/- 7%, p = 0.023) and a trend for higher systolic pulmonary artery pressure (59 +/- 17 mm Hg vs 49 +/- 13 mm Hg, p = 0.08). In cTnI+ patients, the correlation between cTnI levels upon admission and ejection fraction was r = -0.530 (p = 0.11). We found ischemic etiology was equally present in the 2 groups, whereas we never found histologic signs of acute myocarditis. Other clinical characteristics (functional class, daily diuretic dose, need for intravenous inotropes) were not statistically different in the 2 groups. In cTnI+ patients who improved after admission, cTnI became undetectable after a few days; in patients with refractory heart failure who were hospitalized until death, cTnI persisted in detectable levels throughout the observation period. Using the Cox proportional hazard model, a positive cTnI was the most powerful predictor of mortality at 3 months (p = 0.013; hazard ratio 6.86; 95% confidence interval 1.32 to 35.4). CONCLUSIONS: These observations suggest that cTnI is detected in the blood of 25% to 33% of patients with severe heart failure; its presence may help to identify a high-risk sub-group who faces very poor short-term prognosis.
BACKGROUND: Cardiac cell death has been shown to occur in heart failure and has been implicated as one of the mechanisms responsible for progression of the disease. Cardiac Troponin I (cTnI) represents a highly sensitive marker for myocardial cell death. Based on previous studies reporting that cTnI may be detected in patients with heart failure, we evaluated the clinical correlates and prognostic implications of detectable cTnI in a consecutive series of patients with severe heart failure. METHODS: Thirty-four patients were examined. Upon admission, we measured serum levels of cTnI by conventional immunoenzymatic assay (Stratus Dade II). According to the results of this assay, patients were divided into 2 groups, based on the presence (cTnI+) or absence (cTnI-) of detectable cTnI. These 2 groups were compared by non-parametric analysis for their clinical characteristics, instrumental findings, and short-term outcome. RESULTS: The cTnI+ group included 10 patients (29%) with a mean serum cTnI of 0.7 +/- 0.3 ng/ml. Compared with the cTnI- group, these patients had significantly lower left ventricular ejection fractions (20% +/- 5% vs 26% +/- 7%, p = 0.023) and a trend for higher systolic pulmonary artery pressure (59 +/- 17 mm Hg vs 49 +/- 13 mm Hg, p = 0.08). In cTnI+ patients, the correlation between cTnI levels upon admission and ejection fraction was r = -0.530 (p = 0.11). We found ischemic etiology was equally present in the 2 groups, whereas we never found histologic signs of acute myocarditis. Other clinical characteristics (functional class, daily diuretic dose, need for intravenous inotropes) were not statistically different in the 2 groups. In cTnI+ patients who improved after admission, cTnI became undetectable after a few days; in patients with refractory heart failure who were hospitalized until death, cTnI persisted in detectable levels throughout the observation period. Using the Cox proportional hazard model, a positive cTnI was the most powerful predictor of mortality at 3 months (p = 0.013; hazard ratio 6.86; 95% confidence interval 1.32 to 35.4). CONCLUSIONS: These observations suggest that cTnI is detected in the blood of 25% to 33% of patients with severe heart failure; its presence may help to identify a high-risk sub-group who faces very poor short-term prognosis.
Authors: S M Keating; X Deng; F Fernandes; E Cunha-Neto; A L Ribeiro; B Adesina; A I Beyer; P Contestable; B Custer; M P Busch; E C Sabino Journal: Int J Cardiol Date: 2015-07-12 Impact factor: 4.164
Authors: Ziya Kaya; Stefan Göser; Sebastian J Buss; Florian Leuschner; Renate Ottl; Jin Li; Mirko Völkers; Stefan Zittrich; Gabriele Pfitzer; Noel R Rose; Hugo A Katus Journal: Circulation Date: 2008-10-27 Impact factor: 29.690
Authors: L La Vecchia; F Ottani; L Favero; G L Spadaro; A Rubboli; C Boanno; G Mezzena; A Fontanelli; A S Jaffe Journal: Heart Date: 2004-06 Impact factor: 5.994