title: High-sensitivity cardiac troponin-I is elevated in patients with rheumatoid arthritis, independent of cardiovascular risk factors and inflammation.
abstract: OBJECTIVE
  We examined the hypothesis that cardiac-specific troponin-I (cTn-I), a biomarker of myocardial injury, is elevated in patients with rheumatoid arthritis (RA).
  
  
  BACKGROUND
  RA patients have an increased incidence of heart failure (HF). Chronic myocardial injury in RA may be a mechanism for the development of HF.
  
  
  METHODS
  We compared cTn-I concentrations measured by high-sensitivity immunoassay in 164 patients with RA and 90 controls, excluding prior or active heart failure. We examined the relationship between cTn-I concentrations and cardiovascular risk factors, inflammation, and coronary artery calcium score (CACS), a measure of coronary atherosclerosis.
  
  
  RESULTS
  cTn-I concentrations were 49% higher in patients with RA (median 1.15 pg/mL [IQR 0.73-1.92] than controls (0.77 pg/mL [0.49-1.28](P<0.001). The difference remained statistically significant after adjustment for demographic characteristics (P = 0.002), further adjustment for cardiovascular (CV) risk factors (P = 0.004), inflammatory markers (P = 0.008), and in a comprehensive model of CV risk factors and inflammatory markers (P = 0.03). In patients with RA, cTn-I concentrations were positively correlated with age (rho = 0.359), Framingham risk score (FRS) (rho = 0.366), and systolic blood pressure (rho = 0.248 (all P values ≤ 0.001)), but not with measures of inflammation or RA drug therapies. cTn-I was significantly correlated with CACS in RA in univariate analysis, but not after adjustment for age, race, sex and FRS (P = 0.79). Further model adjustments for renal function and coronary artery disease confirmed the significance of the findings.
  
  
  CONCLUSIONS
  High-sensitivity cTn-I concentrations are elevated in patients with RA without heart failure, independent of cardiovascular risk profile and inflammatory markers. Elevated troponin concentrations in RA may indicate subclinical, indolent myocardial injury.
authors: Division of Cardiology, Department of Medicine, Vanderbilt University Medical Center, Nashville, Tennessee, United States of America. william.bradham@vanderbilt.edu
authors: William S
authors: WS
authors: Bradham
authors: Aihua
authors: A
authors: Bian
authors: Annette
authors: A
authors: Oeser
authors: Tebeb
authors: T
authors: Gebretsadik
authors: Ayumi
authors: A
authors: Shintani
authors: Joseph
authors: J
authors: Solus
authors: Joel
authors: J
authors: Estis
authors: Quynh Anh
authors: QA
authors: Lu
authors: John
authors: J
authors: Todd
authors: Paolo
authors: P
authors: Raggi
authors: C Michael
authors: CM
authors: Stein
mesh_terms: D001172:Arthritis, Rheumatoid / Q000150:complications / Q000175:diagnosis* / Q000378:metabolism; D015415:Biomarkers / Q000378:metabolism*; D002114:Calcinosis / Q000175:diagnosis* / Q000209:etiology / Q000378:metabolism; D016022:Case-Control Studies; D003324:Coronary Artery Disease / Q000175:diagnosis* / Q000209:etiology / Q000378:metabolism; D005260:Female; D006333:Heart Failure / Q000175:diagnosis* / Q000209:etiology / Q000378:metabolism; D006801:Humans; D007249:Inflammation / Q000175:diagnosis* / Q000209:etiology / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D011379:Prognosis; D012307:Risk Factors; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D016037:Single-Blind Method; D019210:Troponin I / Q000378:metabolism*
chemical_list: D015415:Biomarkers; D019210:Troponin I