Cardiac Troponin T Measured by a Highly Sensitive Assay Predicts Coronary Heart Disease, Heart Failure, and Mortality in the Atherosclerosis Risk in Communities Study
What is the predictive value of troponin T levels measured by a highly sensitive assay in a general population without apparent cardiovascular disease?
Associations between increasing cardiac troponin T (cTnT) levels and coronary heart disease (CHD), mortality, and heart failure (HF) hospitalization were evaluated with Cox proportional hazards models adjusted for traditional CHD risk factors, kidney function, high-sensitivity C-reactive protein (hs-CRP), and N-terminal pro–B-type natriuretic peptide in 9,698 participants ages 54-74 years, who at baseline were free from CHD and stroke (and HF in the HF analysis).
Measurable cTnT levels (≥0.003 µg/L) were detected in 66.5% of individuals. Those with cTnT levels in the highest category (≥0.014 µg/L; 7.4% of the Atherosclerosis Risk in Communities Study [ARIC] population) had significantly increased risk for CHD (hazard ratio, 2.29), fatal CHD (hazard ratio, 7.59), total mortality (hazard ratio, 3.96), and HF (hazard ratio, 5.95). Even minimally elevated cTnT (≥0.003 µg/L) was associated with increased risk for mortality and HF (p < 0.05). Adding cTnT to traditional risk factors improved risk prediction parameters; the improvements were similar to those with N-terminal pro–B-type natriuretic peptide and better than those with the addition of hs-CRP.
The authors concluded that cTnT detectable with a highly sensitive assay was associated with incident CHD, mortality, and HF in individuals from a general population without known CHD/stroke.
Use of cardiac troponins has improved the diagnosis and management of patients with acute coronary syndrome. The current study adds to previous data demonstrating that even in asymptomatic individuals, subtle elevations of cTnT detected by highly sensitive assays are predictive of future cardiovascular events. Additional studies are necessary to determine the underlying mechanisms by which these low (but elevated) levels of cTnT are generated and how this information can be used to guide therapeutic strategies.
Keywords: Acute Coronary Syndrome, Stroke, Biological Markers, Heart Failure, Troponin T, Coronary Disease, Risk Factors
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