TY - JOUR
T1 - Soluble ST2 is associated with all-cause and cardiovascular mortality in a population-based cohort
T2 - the dallas heart study
AU - Chen, Lu Q.
AU - de Lemos, James A
AU - Das, Sandeep R
AU - Ayers, Colby R.
AU - Rohatgi, Anand K
PY - 2013/3
Y1 - 2013/3
N2 - 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 allcause 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.
AB - 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 allcause 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.
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U2 - 10.1373/clinchem.2012.191106
DO - 10.1373/clinchem.2012.191106
M3 - Article
C2 - 23220272
AN - SCOPUS:84874610413
SN - 0009-9147
VL - 59
SP - 536
EP - 546
JO - Clinical chemistry
JF - Clinical chemistry
IS - 3
ER -