Evidence mapPaperPMID 42428656Full record

ArticleCardiovascular diagnosis and therapy2026

Plasma alarmin S100A8/A9 serves as a potential biomarker of major adverse cardiovascular events after acute myocardial infarction.

Jingjiang Pi, Liang Geng, Chenghui Fan, Jing Xu, Xingxu Wang, Qi Zhang, Wei Wei

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Article in Cardiovascular diagnosis and therapy, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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7 authors.

Jingjiang Pi *Department of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Liang Geng *Department of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Chenghui Fan *Department of Cardiovascular Medicine, State Key Laboratory of Cardiovascular Diseases and Medical Innovation Center, Shanghai East Hospital, School of Medicine, Tongji University, Shanghai, China.
Jing XuDepartment of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Xingxu WangDepartment of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Qi ZhangDepartment of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.
Wei WeiDepartment of Cardiology, Shanghai East Hospital, Tongji University School of Medicine, Shanghai, China.

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6 · The paper itself

Abstract

Background: 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. Methods: 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). Results: 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). Conclusions: 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.

Indexed as

acute myocardial infarction (AMI)all-cause mortalitymajor adverse cardiovascular event (MACE)S100A8/A9

Identifiers

PMID42428656
PMCPMC13345779

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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.