Plasma alarmin S100A8/A9 serves as a potential biomarker of major adverse cardiovascular events after acute myocardial infarction.
S100A8/A9 is a key inflammatory protein significantly upregulated during acute myocardial infarction (AMI). Although previous small-scale studies suggest its potential for cardiovascular risk stratification, its long-term prognostic utility-especially compared to established biomarkers like TnI and BNP-lacks validation in large-scale cohorts. To evaluate the long-term prognostic value of admission plasma S100A8/A9 levels in a large cohort of hospitalized AMI patients, specifically assessing its ability to predict major adverse cardiovascular events (MACE) and its incremental predictive value over traditional clinical models.
This prospective study enrolled 1,312 patients hospitalizing with AMI from August 2013 to June 2016. Plasma S100A8/A9 levels were quantified via ELISA at admission. Multivariable Cox regression and restricted cubic splines were utilized to assess the associations of S100A8/A9 levels with MACE and its components including all-cause mortality, hospitalization for heart failure (HF), and recurrent myocardial infarction (MI).
Over a median follow-up period of 2.93 years, 132 deaths occurred, and 392 patients reached the combined endpoint of MACEs. Even after multivariable adjustment for baseline clinical characteristics and established biomarkers, elevated S100A8/A9 levels remained significantly associated with an increased risk of MACE, all-cause mortality, recurrent MI, and hospitalization for HF (all P for trend <0.001). Furthermore, using Cox model-based Harrell's C-index, discrimination for MACE improved from 0.752 in the reference model to 0.822 after addition of log-transformed S100A8/A9, but not for all-cause mortality, as reflected in C-index (0.718 to 0.720), with bootstrap ΔC-index 0.002 (95% CI: -0.005, 0.013; P=0.58).
Plasma S100A8/A9 concentrations demonstrate a strong correlation with heightened risk of MACE in AMI patients. Notably, the prognostic value of S100A8/A9 is significantly more pronounced for composite cardiovascular outcomes (MACE) compared to all-cause mortality. These findings indicate that S100A8/A9 serves as a valuable novel biomarker to guide targeted risk stratification of post-AMI patients.
This prospective study enrolled 1,312 patients hospitalizing with AMI from August 2013 to June 2016. Plasma S100A8/A9 levels were quantified via ELISA at admission. Multivariable Cox regression and restricted cubic splines were utilized to assess the associations of S100A8/A9 levels with MACE and its components including all-cause mortality, hospitalization for heart failure (HF), and recurrent myocardial infarction (MI).
Over a median follow-up period of 2.93 years, 132 deaths occurred, and 392 patients reached the combined endpoint of MACEs. Even after multivariable adjustment for baseline clinical characteristics and established biomarkers, elevated S100A8/A9 levels remained significantly associated with an increased risk of MACE, all-cause mortality, recurrent MI, and hospitalization for HF (all P for trend <0.001). Furthermore, using Cox model-based Harrell's C-index, discrimination for MACE improved from 0.752 in the reference model to 0.822 after addition of log-transformed S100A8/A9, but not for all-cause mortality, as reflected in C-index (0.718 to 0.720), with bootstrap ΔC-index 0.002 (95% CI: -0.005, 0.013; P=0.58).
Plasma S100A8/A9 concentrations demonstrate a strong correlation with heightened risk of MACE in AMI patients. Notably, the prognostic value of S100A8/A9 is significantly more pronounced for composite cardiovascular outcomes (MACE) compared to all-cause mortality. These findings indicate that S100A8/A9 serves as a valuable novel biomarker to guide targeted risk stratification of post-AMI patients.