Association of troponin T detected with a highly sensitive assay and cardiac structure and mortality risk in the general population.
BACKGROUND
Detectable levels of cardiac troponin T (cTnT) are strongly associated with structural heart disease and increased risk of death and adverse cardiovascular events; however, cTnT is rarely detectable in the general population using standard assays.


OBJECTIVE
To determine the prevalence and determinants of detectable cTnT in the population using a new highly sensitive assay and to assess whether cTnT levels measured with the new assay associate with pathological cardiac phenotypes and subsequent mortality.


METHODS
Cardiac troponin T levels were measured using both the standard and the highly sensitive assays in 3546 individuals aged 30 to 65 years enrolled between 2000 and 2002 in the Dallas Heart Study, a multiethnic, population-based cohort study. Mortality follow-up was complete through 2007. Participants were placed into 5 categories based on cTnT levels.


METHODS
Magnetic resonance imaging measurements of cardiac structure and function and mortality through a median of 6.4 (interquartile range, 6.0-6.8) years of follow-up.


RESULTS
In Dallas County, the prevalence of detectable cTnT (≥0.003 ng/mL) was 25.0% (95% confidence interval [CI], 22.7%-27.4%) with the highly sensitive assay vs 0.7% (95% CI, 0.3%-1.1%) with the standard assay. Prevalence was 37.1% (95% CI, 33.3%-41.0%) in men vs 12.9% (95% CI, 10.6%-15.2%) in women and 14.0% (95% CI, 11.2%-16.9%) in participants younger than 40 years vs 57.6% (95% CI, 47.0%-68.2%) in those 60 years and older. Prevalence of left ventricular hypertrophy increased from 7.5% (95% CI, 6.4%-8.8%) in the lowest cTnT category (<0.003 ng/mL) to 48.1% (95% CI, 36.7%-59.6%) in the highest (≥0.014 ng/mL) (P < .001); prevalence of left ventricular systolic dysfunction and chronic kidney disease also increased across categories (P < .001 for each). During a median follow-up of 6.4 years, there were 151 total deaths, including 62 cardiovascular disease deaths. All-cause mortality increased from 1.9% (95% CI, 1.5%-2.6%) to 28.4% (95% CI, 21.0%-37.8%) across higher cTnT categories (P < .001). After adjustment for traditional risk factors, C-reactive protein level, chronic kidney disease, and N-terminal pro-brain-type natriuretic peptide level, cTnT category remained independently associated with all-cause mortality (adjusted hazard ratio, 2.8 [95% CI, 1.4-5.2] in the highest category). Adding cTnT categories to the fully adjusted mortality model modestly improved model fit (P = .02) and the integrated discrimination index (0.010 [95% CI, 0.002-0.018]; P = .01).


CONCLUSIONS
In this population-based cohort, cTnT detected with a highly sensitive assay was associated with structural heart disease and subsequent risk for all-cause mortality.
Division of Cardiology, University of Texas Southwestern Medical Center, 5909 Harry Hines Blvd, Dallas, TX 75390-9047, USA. james.delemos@utsouthwestern.edu
James A
JA
de Lemos
Mark H
MH
Drazner
Torbjorn
T
Omland
Colby R
CR
Ayers
Amit
A
Khera
Anand
A
Rohatgi
Ibrahim
I
Hashim
Jarett D
JD
Berry
Sandeep R
SR
Das
David A
DA
Morrow
Darren K
DK
McGuire
D000328:Adult; D000368:Aged; D015331:Cohort Studies; D005260:Female; D006331:Heart Diseases / Q000097:blood* / Q000401:mortality*; D006801:Humans; D008279:Magnetic Resonance Imaging; D008297:Male; D008875:Middle Aged; D009026:Mortality / Q000639:trends; D009206:Myocardium / Q000473:pathology*; D010641:Phenotype; D015995:Prevalence; D012306:Risk; D012680:Sensitivity and Specificity; D013781:Texas / Q000453:epidemiology; D020107:Troponin T / Q000097:blood*
D020107:Troponin T