Abstract P010: Cardiac Risk Factors and 6-Year Change in high-sensitivity Cardiac Troponin-T.

Abstract

Introduction: Troponin measured with a highly sensitive assay (hs-cTNT) can detect subclinical myocardial injury and may be useful for risk stratification. However, little is known about temporal changes in hs-cTNT in the general population. Hypothesis: Traditional cardiac risk factors will predict change in hs cTNT. Methods: We analyzed data from 8698 ARIC Study participants, free of cardiovascular disease, who had hs-cTNT measured at visit 2 (1990-1992) and visit 4 (1996-1998). Hs-cTNT was categorized as: undetectable (<5 ng/L), detectable (5-14 ng/L), and elevated (≥14 ng/L). We examined the association of baseline Framingham Risk Score (FRS) groups (low <10%, intermediate 10-20%, high >20%) and individual cardiac risk factors with change across hs-cTNT categories using Poisson regression and with absolute 6-year change using robust linear regression. Results: Over 6 years, 2124 study participants went from undetectable to detectable or elevated hs-cTNT and 353 went from detectable to elevated hs-cTNT. The mean crude 6-year hs-cTNT change (SD) within FRS groups were; low (+1.3 (6.0) ng/L), intermediate (+2.3 (9.3) ng/L), and high (+3.7 (8.3) ng/L). Higher baseline FRS was associated with an increase in hs-cTNT over 6 years ( Table ). This association was stronger for incident detectable hs-cTNT than for progression from detectable to elevated. Major predictors of change were baseline age, male gender, diabetes and hypertension. Black race/ethnicity and obesity were also associated with categorical hs-cTNT change. In addition to HDL-c, baseline hypercholesterolemia and smoking may be associated with downwards hs-cTNT change. Conclusions: Framingham Risk Score was positively associated with 6-year hs-cTNT change in middle-age adults. The modifiable risk factors primarily driving this association were diabetes, hypertension, and obesity. Additional studies are needed to evaluate if modifying these risk factors can prevent progression of subclinical myocardial damage.