Cardiac troponin I as diagnostic and prognostic marker in severe heart failure

Citation
L. La Vecchia et al., Cardiac troponin I as diagnostic and prognostic marker in severe heart failure, J HEART LUN, 19(7), 2000, pp. 644-652
Citations number
45
Categorie Soggetti
Cardiovascular & Respiratory Systems
Journal title
JOURNAL OF HEART AND LUNG TRANSPLANTATION
ISSN journal
10532498 → ACNP
Volume
19
Issue
7
Year of publication
2000
Pages
644 - 652
Database
ISI
SICI code
1053-2498(200007)19:7<644:CTIADA>2.0.ZU;2-A
Abstract
Background: Cardiac cell death has been shown to occur in heart failure and has been implicated as one of the mechanisms responsible for progression o f the disease. Cardiac Troponin I (cTnI) represents a highly sensitive mark er 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 se rum levels of cTnI by conventional immunoenzymatic assay (Stratus Dade II). According to the results of this assay, patients were divided into 2 group s, based on the presence (cTnI+) or absence (cTnI-) of detectable cTnI, The se 2 groups were compared by non-parametric analysis for their clinical cha racteristics, 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 sig nificantly 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). Tn cTnI+ patients, the corre lation 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 gro ups, whereas we never found histologic signs of acute myocarditis. Other cl inical characteristics (functional class, daily diuretic dose, need for int ravenous inotropes) were not statistically different in the 2 groups, In cT nI+ 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 m ost 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.