Six-Year Change in High-Sensitivity Cardiac Troponin T and Risk of Subsequent Coronary Heart Disease, Heart Failure,
John W McEvoy1, Yuan Chen2, Chiadi E Ndumele1
1Department of Epidemiology and the Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland2Ciccarone Center for the Prevention of Heart Disease, Department of Medicine, Johns H.
Insights
Tracking changes in high-sensitivity cardiac troponin T (hs-cTnT) over time predicts future cardiovascular events. Serial hs-cTnT measurements offer valuable prognostic information for identifying high-risk individuals.
Area of Science:
- Cardiology
- Biomarker Research
- Preventive Medicine
Background:
- High-sensitivity cardiac troponin T (hs-cTnT) is a key cardiovascular risk biomarker.
- Limited data exist on long-term hs-cTnT changes and outcomes, especially in primary prevention.
Purpose of the Study:
- To evaluate the association between 6-year changes in hs-cTnT and incident coronary heart disease (CHD), heart failure (HF), and all-cause mortality.
- To assess the added prognostic value of hs-cTnT change to existing risk models.
Main Methods:
- Prospective observational cohort study (1990-2011) of 8838 participants from the Atherosclerosis Risk in Communities Study.
- hs-cTnT measured at baseline and 6-year follow-up; Cox proportional hazards regression used to analyze outcomes over 16 years.
- Harrell C statistic assessed improvement in risk discrimination.
Main Results:
- Incident detectable hs-cTnT was linked to increased risk of CHD, HF, and death.
- Significant increases in hs-cTnT (e.g., <0.005 to ≥0.014 ng/mL) were associated with substantially higher hazard ratios for CHD, HF, and mortality.
- Reductions in hs-cTnT >50% were associated with lower subsequent risks.
- hs-cTnT change improved prediction of HF and death beyond traditional factors and baseline hs-cTnT.
Conclusions:
- Progressive increases in hs-cTnT indicate ongoing myocardial damage and are independently associated with higher risks of CHD, HF, and death.
- Serial hs-cTnT measurements provide clinically relevant prognostic information.
- Tracking hs-cTnT trajectory aids in risk stratification and targeted prevention, particularly for individuals with early-stage HF.
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 data were 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.
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