Abstract
Background: Ongoing myocardial cell damage forms the basis for progression of chronic heart failure. Evidence is accumulating that progressive loss of cardiac myocytes is associated with the release of cardiac troponin I (cTnI).
Hypothesis: This study sought to determine whether levels of cTnI are of prognostic value for risk stratification of patients with chronic heart failure.
Methods: Release of cTnI was measured by conventional enzyme immunoassay following serum ultrafiltration in 58 consecutive patients hospitalized for chronic heart failure and 31 healthy volunteers serving as control group. Determination of serum levels was performed every 2 weeks over a time interval of 3 months. According to the results of coronary angiography, patients were divided into Group D showing normal coronary arteries (n = 33, ejection fraction 27 ± 6.1%) and Group I showing severe coronary heart disease (n = 25, ejection fraction 28.8 ± 7.8%). Survival of patients was evaluated after a mean time interval of 3 years.
Results: The mean cTnI serum level over all measurements was 0.66 ± 1.8 ng/ml in patients versus 0.11 ± 0.48 ng/ml in volunteers. At all six points of analysis, the mean cTnI serum level was significantly different (p < 0.001) between patients and volunteers. There was no significant difference between patients with and without coronary heart disease following hospital discharge, however, troponin release was significantly different between survivors and nonsurvivors (n = 27) (0.56 ng/ml vs. 0.84 ng/ml; p < 0.05).
Conclusion: Permanent cTnI release is a common finding in patients with chronic heart failure and a strong prognosticator. In this setting, coronary morphology seems to play a minor role for disease progression.
Keywords: cardiac function, cardiovascular anatomy, cardiovascular biochemistry, cardiovascular pathology, clinical trials, heart failure, ischemic heart disease, troponin, trigger event
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