title: Soluble ST2 is associated with all-cause and cardiovascular mortality in a population-based cohort: the Dallas Heart Study.
abstract: BACKGROUND
  ST2, part of the interleukin-1 receptor family, is released from cardiac myocytes under mechanical strain. Soluble ST2 (sST2) concentrations are associated with adverse cardiac events in high-risk cohorts. We evaluated the association of sST2 with all-cause and cardiovascular mortality in a large, low-risk population-based cohort.
  
  
  METHODS
  Plasma sST2 was measured in 3294 subjects from the Dallas Heart Study, a probability-based population cohort. We categorized participants into undetectable (reference group) or quartiles of detectable sST2 concentrations. Associations with all-cause and cardiovascular mortality were assessed over a median 8.3 years of follow-up.
  
  
  RESULTS
  sST2 concentrations were not significantly associated with most traditional risk factors, prevalent subclinical cardiovascular disease, or nonfatal cardiac events. However, a higher proportion of African Americans had detectable concentrations of sST2 than non-African Americans (44% vs 21%, respectively, P < 0.0001). In addition, sST2 concentrations were significantly associated with markers of inflammation. Increased sST2 was associated with increased all-cause mortality (Ptrend ≤ 0.0001) and cardiovascular mortality (Ptrend = 0.0004). In fully adjusted models, those in the highest quartile of detectable sST2 were at increased risk for all-cause death compared to those with undetectable sST2 concentrations (adjusted hazard ratio 2.1, 95% CI 1.4-3.2, P = 0.0009).
  
  
  CONCLUSIONS
  In a low-risk population, sST2 does not associate with traditional cardiovascular risk factors or nonfatal cardiovascular events but is higher in African Americans and is associated with increased all-cause and cardiovascular mortality. Further investigation is needed regarding the role of sST2 in risk prediction, particularly among African Americans.
authors.affiliation: Department of Internal Medicine, Donald W. Reynolds Cardiovascular Research Center, Dallas, TX, USA.
authors.forename: Lu Q
authors.initials: LQ
authors.lastname: Chen
authors.forename: James A
authors.initials: JA
authors.lastname: de Lemos
authors.forename: Sandeep R
authors.initials: SR
authors.lastname: Das
authors.forename: Colby R
authors.initials: CR
authors.lastname: Ayers
authors.forename: Anand
authors.initials: A
authors.lastname: Rohatgi
mesh_terms: D000328:Adult; D001741:Black or African American; D000368:Aged; D015415:Biomarkers; D002318:Cardiovascular Diseases / Q000097:blood / Q000208:ethnology / Q000401:mortality*; D015331:Cohort Studies; D005260:Female; D006801:Humans; D000072179:Interleukin-1 Receptor-Like 1 Protein; D008297:Male; D008875:Middle Aged; D016016:Proportional Hazards Models; D011956:Receptors, Cell Surface / Q000097:blood* / Q000502:physiology; D012307:Risk Factors
chemical_list: D015415:Biomarkers; C079241:IL1RL1 protein, human; D000072179:Interleukin-1 Receptor-Like 1 Protein; D011956:Receptors, Cell Surface