Association Of Troponin T Measured By A Highly Sensitive Assay And Cardiovascular Events In Community-Dwelling Population

Background:A high-sensitivity assay for cardiac troponin T (hs-cTnT) has recently become available; this assay detects low troponin concentrations and improves precision at the lower limit of detection. Very low circulating levels of troponin are detectable in the general population with the new generation assays, yet the clinical significance and determinants of detectable hs-cTnT in the general population is not known. Albuminuria is an important predictor of adverse cardiovascular events, whether albuminuria is associated with the release of very low levels of cTnT in asymptomatic subjects remains to be established.Mathods:Baseline cTnT levels were measured using the highly sensitive assays in 1631 individuals (mean aged 62.4 years,58.1% female) who were free from cardiovascular diseases (CVD) enrolled between 2007 and 2009 in a community-based study. New onset mortality and cardiovascular events follow-up were complete through 2013. We measured hs-cTnT again and also detected urine albumin/creatinine ratio (UACR) in the same year. We assessed both the cross-sectional associations of hs-cTnT to cardiovascular risk factors and the longitudinal associations to outcomes over follow-up. Associations between increasing hs-cTnT levels and outcomes. were evaluated with Cox proportional hazards models adjusted for multiple risk factors.Results:Measurable hs-cTnT levels were detected in 54.6% of individuals,11.4% of subjects had elevated hs-cTnT (≥14 pg/mL). In multivariable logistic regression analysis, age, male sex, diabetes mellitus and lower estimated glomerular filtration rate were independently associated with presence of detectable or elevated hs-cTnT. In addition, UACR level was an independent predictor of hs-cTnT (Standardized β=0.102, P<0.001). UACR (odds ratio:1.40; 95% CI:1.08 tol.65; P=0.002) was associated with a higher likelihood of elevated hs-cTnT. A fully adjusted logistic analysis revealed that compared with participants in the lowest UACR quartile, those in the highest quartile had a 2.43-fold (95% CI:1.25 to 5.08; P= 0.006) increased risk of elevated hs-cTnT. During a mean follow-up of 4.8 years, there were 52 deaths, including 24 cardiovascular disease deaths.154 participants experienced new-onset major cardiovascular events,99 subjects had coronary events, and 61 strokes of all kinds occurred. In multivariable adjusted models, the hs-cTnT levels were associated with each end point except stroke. In fully adjusted models, compared with participants with undetectable levels, those with hs-cTnT levels in the highest category (>14 pg/mL) had significantly increased risk for all-cause mortality (hazard ratio [HR]= 2.07; 95% confidence interval[CI],1.05 to 3.01), cardiovascular mortality (HR= 2.71; 95% CI, 1.42 to 7.03), cardiovascular events (HR= 3.27; 95% CI,1.88 to 5.70), and coronary events (HR= 4.50; 95% CI,2.26 to 9.02). Even minimally elevated hs-cTnT (>6.22 pg/mL) was associated with increased risk for cardiovascular and coronary events (P<0.01). Both dynamic relative change and absolute change in hs-cTnT were significantly associated with higher cardiovascular events risk after adjustment for conventional risk factors, baseline levels of hs-cTnT and N-terminal pro-brain natriuretic peptide. Among individuals with initially detectable hs-cTnT, a subsequent increase of more than 50% was associated with a greater risk for cardiovascular events (HR= 1.65; 95% CI,1.04 to 2.63) and coronary events (HR= 1.76; 95% CI,1.10 to 2.86) compared with participants with 50% or less change.Conclusions:In this community-based cohort without known CVD, baseline and changes in cTnT levels measured with a highly sensitive assay were significantly associated with subsequent risk for mortality, cardiovascular events and might support selection of at risk individuals. Higher urine albumin excretion is associated with elevated hs-cTnT among the general population, suggesting that albuminuria contributes to subclinical myocardial damage beyond its effects on the development of vascular endothelial dysfunction.