Troponin T Change and Risk of CHD, HF, and Death
What is the association of 6-year change in high-sensitivity cardiac troponin T (hs-cTnT) with incident coronary heart disease (CHD), heart failure (HF), and all-cause mortality?
This prospective observational cohort study, performed from January 1, 1990, to December 31, 2011, included 8,838 participants with biracial representation from the Atherosclerosis Risk in Communities Study who were initially free of CHD and HF and who had hs-cTnT measured twice, 6 years apart. Risk factor and temporal hs-cTnT data were collected. Using Cox proportional hazards regression, the investigators examined the association of hs-cTnT change with subsequent CHD, HF, and death during a maximum of 16 years. Improvement in discrimination was determined by the Harrell C statistic.
Of the 8,838 participants (mean age, 56 years; 5,215 female [59.0%]; 1,891 black [21.4%]), there were 1,157 CHD events, 965 HF events, and 1,813 deaths overall. Incident detectable hs-cTnT (baseline, <0.005 ng/ml; follow-up, ≥0.005 ng/ml) was independently associated with subsequent CHD (hazard ratio [HR], 1.4; 95% confidence interval [CI], 1.2-1.6), HF (HR, 2.0; 95% CI, 1.6-2.4), and death (HR, 1.5; 95% CI, 1.3-1.7), relative to an hs-cTnT level <0.005 ng/ml at both visits. In addition, HRs as high as 4 for CHD and death and 8 for HF were recorded among individuals with the most marked hs-cTnT increases (e.g., baseline, <0.005 ng/ml; follow-up, ≥0.014 ng/ml). Risk for subsequent outcomes was lower among those with relative hs-cTnT reductions >50% from baseline. Furthermore, information on hs-cTnT change improved discrimination for HF and death when added to a model that included traditional risk factors, N-terminal pro–brain natriuretic peptide, and baseline hs-cTnT level. Among individuals with adjudicated HF hospitalizations, hs-cTnT change appeared to be similarly associated with HF with reduced and preserved ejection fraction.
The authors concluded that temporal increases in hs-cTnT, suggestive of progressive myocardial damage, are independently associated with incident CHD, death, and, above all, HF.
This study reports that temporal increases in hs-cTnT were independently associated with incident CHD, death, and HF events in this prospective biracial sample of middle-aged adults. These results indicate that two measurements of hs-cTnT may be better than a single value for characterizing risk, and that large increases in hs-cTnT are particularly deleterious. Temporal change in hs-cTnT may help guide the future preventive management of asymptomatic persons at risk for CHD and adults with stage A or B HF. We need trials to optimize treatment for medical conditions associated with hs-cTnT elevation, and of potential therapies that may provide cardioprotection in those with temporal increases in hs-cTnT.
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