Troponin T Predicts Death and Heart Failure Risk in Stable CHD Patients

November 27, 2009

November 27, 2009 (Lorenskog, Norway) — Very low circulating levels of cardiac troponin T are detectable in the great majority of patients with stable coronary heart disease and have a graded relationship with the incidence of cardiovascular death and heart failure, but not with MI, a new analysis from the PEACE study shows [1].

The study, published online November 25, 2009 in the New England Journal of Medicine, is authored by a group led by Dr Torbjorn Omland (Akershus University Hospital, Lorenskog, Norway).

Omland told heartwire that this is the first time that very low levels of troponin T have been investigated as a marker of risk in this population. "Troponin is associated with a large number of traditional risk factors, including age, sex, previous MI, diabetes, and hypertension. This measurement is probably integrating information from many risk factors. The clinical implications of our study are not yet known, but the results suggest that assessment of low-level chronic myocardial injury might represent a new means by which risk can be stratified among patients with stable CHD", he said.

The authors explain that raised troponin levels are strongly associated with recurrent events in patients with unstable coronary disease, but their prognostic value in patients with stable heart disease has not been investigated.

They note that detection of troponin has been linked to adverse outcomes in healthy volunteers and in patients with recent ACS. Using a new highly sensitive assay that enables the measurement of troponin T concentrations that are lower by a factor of 10 than those measurable with previous assays, Omland et al investigated whether cardiac troponin T was detectable in patients with stable CHD without heart failure and whether these levels were associated with the risk of future cardiovascular events.

They analyzed troponin T levels from blood samples taken from 3593 patients with stable CHD participating in the PEACE trial. Results of the assay were analyzed in relation to the incidence of cardiovascular events during a mean follow-up period of 5.2 years.

Results showed that, with the highly sensitive assay, concentrations of cardiac troponin T were at or above the limit of detection (0.001 μg/L) in 97.7% of patients and at or above the 99th percentile for apparently healthy subjects (0.0133 μg/L) in 11.1% of patients.

After adjustment for other independent prognostic indicators, there was a strong and graded increase in the cumulative incidence of cardiovascular death and of heart failure. However, there was no association between troponin T levels, measured with the highly sensitive assay, and the incidence of MI.

Association Between High-Sensitivity Cardiac Troponin T and Cardiovascular Outcomes*

Outcome Hazard Ratio (95% CI) P
CV death 2.09 (1.60-2.74) <0.001
Fatal or nonfatal CHF 2.20 (1.66-2.90) <0.001
Fatal or nonfatal MI 1.16 (0.97-1.40) 0.11

*Results adjusted for treatment assignment, age, sex, smoking status, CRP, and NT-pro BNP. The hazard ratio is for each unit increase in the natural logarithm of the high-sensitivity cardiac troponin T level.

Omland told heartwire that adding troponin T to the model of traditional risk factors plus CRP and NT-pro BNP modestly but significantly increased the C statistic, suggesting that measuring troponin T adds additional prognostic information.

The authors note that with the use of conventional assays, the prevalence of detectable concentrations of cardiac troponin T in the general population is about 0.7%, and these patients would have established cardiovascular disease or high-risk conditions, such as renal disease or diabetes.

They suggest that the mechanisms responsible for the release of very low levels of cardiac troponin T in patients with stable CHD could include transient clinically silent ischemic episodes and small vessel occlusions, inflammatory processes, cardiomyocyte apoptosis, reduced renal clearance, and increased myocardial strain due to pressure or volume overload. They add that the remarkably high prevalence of detectable troponin in this low-risk cohort raises the possibility that some troponin circulates under normal circumstances in human plasma.

Omland described the finding that troponin T did not predict MI in this study as "surprising," given that in the acute setting troponins are a strong predictor of risk. "This may suggest that the mechanisms may be different in the acute and stable settings," he said.

  1. Omland T, de Lemos J, Sabatine MS, et al. A sensitive cardiac troponin T assay in stable coronary artery disease. N Engl J Med 2009; DOI: 10.1056/NEJMoa0805299. Abstract


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