title: Six-Year Change in High-Sensitivity Cardiac Troponin T and Risk of Subsequent Coronary Heart Disease, Heart Failure, and Death.
abstract: 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.
  
  
  
  To examine the association of 6-year change in hs-cTnT with incident coronary heart disease (CHD), heart failure (HF), and all-cause mortality.
  
  
  
  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.
  
  
  
  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.
  
  
  
  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.
  
  
  
  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.
authors.affiliation: Department 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.
authors.forename: John W
authors.initials: JW
authors.lastname: McEvoy
authors.affiliation: Department of Epidemiology and the Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
authors.forename: Yuan
authors.initials: Y
authors.lastname: Chen
authors.affiliation: Department 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.
authors.forename: Chiadi E
authors.initials: CE
authors.lastname: Ndumele
authors.affiliation: Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital, Boston, Massachusetts.
authors.forename: Scott D
authors.initials: SD
authors.lastname: Solomon
authors.affiliation: Michael E DeBakey Veterans Affairs Hospital, Houston, Texas5Department of Medicine, Section of Cardiovascular Research, Baylor College of Medicine, Houston, Texas6Houston Methodist DeBakey Heart and Vascular Center, Houston, Texas.
authors.forename: Vijay
authors.initials: V
authors.lastname: Nambi
authors.affiliation: Department of Medicine, Section of Cardiovascular Research, Baylor College of Medicine, Houston, Texas6Houston Methodist DeBakey Heart and Vascular Center, Houston, Texas.
authors.forename: Christie M
authors.initials: CM
authors.lastname: Ballantyne
authors.affiliation: Ciccarone Center for the Prevention of Heart Disease, Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland.
authors.forename: Roger S
authors.initials: RS
authors.lastname: Blumenthal
authors.affiliation: Department of Epidemiology and the Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
authors.forename: Josef
authors.initials: J
authors.lastname: Coresh
authors.affiliation: Department of Epidemiology and the Welch Center for Prevention, Epidemiology, and Clinical Research, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland.
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Selvin
mesh_terms: D015415:Biomarkers / Q000378:metabolism*; D003327:Coronary Disease / Q000401:mortality*; D005260:Female; D006333:Heart Failure / Q000401:mortality*; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D020107:Troponin T / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D020107:Troponin T