Home > Uncategorized > Longitudinal Troponin T Changes Predictors of Mortality, Coronary Heart Disease and Heart Failure

Longitudinal Troponin T Changes Predictors of Mortality, Coronary Heart Disease and Heart Failure

McEvoy et al report a six year community prospective observational study assessing the relationship between changes in high-sensitivity troponin T and cardiovascular events (coronary heart disease, heart failure) and mortality.

Summary

IMPORTANCE

High-sensitivity cardiac troponin T (hs-cTnT) is a biomarker of cardiovascular risk and could be approved in the United States for clinical use soon. However, data linking long-term temporal change in hs-cTnT to outcomes are limited, particularly in primary prevention settings.

OBJECTIVE

To examine the association of 6-year change in hs-cTnT with incident coronary heart disease (CHD), heart failure (HF), and all-cause mortality.

DESIGN, SETTING, AND PARTICIPANTS

This prospective observational cohort study, performed from January 1, 1990, to December 31, 2011, included 8838 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. Data analysis was performed from October 28, 2014, to March 9, 2016.

MAIN OUTCOME AND MEASURES

Risk factor and temporal hs-cTnT datawere collected. Using Cox proportional hazards regression, we 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.

RESULTS

Of the 8838 participants (mean age, 56 years; 5215 female [59.0%]; 1891 black [21.4%]) there were 1157 CHD events, 965 HF events, and 1813 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%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 less than 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 (eg, baseline, < 0.005 ng/mL; follow-up,0.014 ng/mL). Risk for subsequent outcomes was lower among those with relative hs-cTnT reductions greater than 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.

CONCLUSIONS AND RELEVANCE

Temporal increases in hs-cTnT, suggestive of progressive myocardial damage, are independently associated with incident CHD, death, and, above all, HF. Serial determination of hs-cTnT trajectory adds clinically relevant information to baseline
testing and may be useful in prognostic assessments and the targeting of prevention strategies to high-risk individuals, especially among persons with stage A or B HF.

The editorial is available here.

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