© 2008 European Society of Cardiology
Clinical significance of cardiac troponins I and T in acute heart failure
a Department of Internal Medicine, Kanta-Hame Central Hospital Finland
b Divisions of Cardiology and Emergency Care, Helsinki University Central Hospital Finland
c Department of Medicine, Central Finland Central Hospital Finland
d Department of Cardiology, Kuopio University Hospital Finland
e Department of Clinical Chemistry, Helsinki University Finland
f Department of Surgery, Helsinki University Central Hospital Finland
g Department of Medicine, Turku University Central Hospital Finland
* Tel.: +358 50 5826979. E-mail address: tuomo.ilva{at}pp.inet.fi
| Abstract |
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Background: Elevated cardiac troponin (cTn) levels are relatively common in acute heart failure (AHF).
Aims: To evaluate the prevalence and prognostic significance of elevated cTnI and cTnT in AHF.
Methods: FINN-AKVA is a prospective, multicenter study in AHF. In this analysis, 364 non-ACS patients with measurements of cTnI and cTnT taken on admission and 48 h thereafter were analyzed.
Results: Of the 364 AHF patients, 51.1% had cTnI and 29.7% cTnT levels above the cut-off value. Six-month all-cause mortality was 18.7%. Both cTnI (OR 2.0, 95% CI 1.2–3.5, p=0.01) and cTnT (OR 2.6, 95% CI 1.5–4.4, p=0.0006) were associated with adverse outcome. The mortality risk was proportional to the magnitude of cTn release. On multivariable analysis, Cystatin C (OR 6.3, 95% CI 3.2–13, p<0.0001), logNT-proBNP (OR 1.4, 95% CI 1.0–1.8, p=0.03) and systolic blood pressure on admission (/10 mm Hg increase, OR 0.9, 95% CI 0.8–0.9, p=0.0004) were independent risk markers, whereas the troponins were not significantly associated with increased mortality.
Conclusions: cTn elevations are frequent in AHF patients without ACS. cTnI is more often elevated than cTnT. Both cTnI and cTnT elevations are associated with increased mortality proportional to the degree elevation but they do not act as independent risk markers.
Key Words: Acute heart failure Troponin I Troponin T Prognosis
Received December 27, 2007; Revised April 27, 2008; Accepted June 9, 2008