Patterns and determinants of temporal change in high-sensitivity cardiac troponin-T: The Atherosclerosis Risk in Communities Cohort Study

Background: Patterns and determinants of temporal change in highly-sensitivity troponin-T (hs-cTNT), a novel measure of subclinical myocardial injury, among asymptomatic persons have not been well characterized.

Methods: We studied 8571 ARIC Study participants, free of cardiovascular disease, who had hs-cTNT measured at two time-points, 6 years apart (1990-1992 and 1996-1998). We examined the association of baseline 10-year atherosclerotic cardiovascular (ASCVD) risk-group (<5%, 5-7.4%, ≥ 7.5%) and individual cardiac risk-factors with change across hs-cTNT categories using Poisson and Multinomial Logistic regression and with mean continuous hs-cTNT change using linear regression.

Results: Mean age was 57 years and 43% were male. Mean (SD) 6-year hs-cTNT change was higher across increasing ASCVD risk-groups; +1.2 (6.1) ng/L [<5%], +2.1 (5.4) ng/L [5-7.4%], and +2.8 (8.8) ng/L [≥ 7.5%]. Major baseline determinants of temporal hs-cTNT increases were: age, male gender, hypertension, diabetes, and obesity. In addition, the relative risk (RR) of incident elevated hs-cTNT (≥ 14 ng/L) was 1.46 (95% CI 1.1-2.0) for persons with sustained hypertension compared to those who remained normotensive. Results for sustained obesity (RR 1.65 [1.19-2.29]) and hyperglycemia (RR 1.76 [1.16-2.67]) were similar. These associations were generally stronger after accounting for survival bias. However, smoking, LDL-cholesterol and triglycerides were not associated with hs-cTNT change. HDL-cholesterol was associated with declining hs-cTNT.

Conclusions: Persons in higher ASCVD risk-groups were more likely to have increases in hs-cTNT over 6 years of follow-up. The modifiable risk-factors primarily driving this association were diabetes, hypertension, and obesity; particularly when they were persistently elevated over follow-up. Future studies are needed to determine whether modifying these risk factors can prevent progression of subclinical myocardial injury.