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Original article
ST2 may not be a useful predictor for incident cardiovascular events, heart failure and mortality
  1. Maria F Hughes1,2,4,5,
  2. Sebastian Appelbaum1,2,
  3. Aki S Havulinna3,
  4. Annika Jagodzinski1,2,
  5. Tanja Zeller1,2,
  6. Frank Kee4,
  7. Stefan Blankenberg1,2,
  8. Veikko Salomaa3
  9. on behalf of the FINRISK and BiomarCaRE investigators
  1. 1Department of General and Interventional Cardiology, Hamburg University Heart Center, Hamburg, Germany
  2. 2German Center for Cardiovascular Research (DZHK), Partner Site Hamburg/Lübeck/Kiel, Germany
  3. 3Department of Chronic Disease Prevention, National Institute for Health and Welfare, Helsinki, Finland
  4. 4Centre of Excellence for Public Health Northern Ireland, Queens University Belfast, Belfast, UK
  5. 5MRC Epidemiology Unit, University of Cambridge, Cambridge, UK
  1. Correspondence to Dr Maria Hughes, UKCRC Centre of Excellence for Public Health Research Northern Ireland, School of Medicine, Dentistry and Biomedical Sciences, Institute of Clinical Sciences B, Queens University Belfast, Grosvenor Road, Belfast BT126BJ, UK;{at}


Objectives We hypothesised that soluble ST2 (sST2) levels can identify people with elevated risk of subsequent cardiovascular disease (CVD) and add to existing risk prediction algorithms.

Background ST2 is a receptor for the inflammatory cytokine IL33. Increased sST2 levels have been associated with heart failure and death in acute myocardial infarction patients and in the general population.

Methods We measured high-sensitivity sST2 in 8444 men and women (25–74 years) from the FINRISK97 prospective population cohort. Cox proportional hazards modelling evaluated the ability of sST2 to predict fatal and non-fatal heart failure, CVD (coronary heart disease, stroke), diabetes, and death over 15 years follow-up. Discrimination and reclassification statistics for 10-year absolute risks compared the ability of sST2 to improve upon Framingham risk factors (FRF), N-terminal pro-brain natriuretic peptide (NT-proBNP), renal function (eGFR) and prevalent valvular heart disease (VHD).

Results sST2 showed suggestive but non-significant associations with heart failure {(HR per 1 SD of log sST2 1.06; 95% CI 0.96 to 1.17 (562 events))}, and with CVD (1.01 95% CI 0.94 to 1.08) (914 events) after adjustment for FRF, NT-proBNP, eGFR and VHD. sST2 significantly predicted death from all causes following similar adjustment ({HR 1.09 (95% CI 1.01 to 1.19) (974 events))}. No improvement in the c-index was observed for models adding sST2 to the risk factors.

Conclusions In a healthy general population from Finland, sST2 did not improve long-term prediction of cardiovascular events including heart failure or all-cause mortality.


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