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S100A8/A9 as a prognostic biomarker with causal effects for post-acute myocardial infarction heart failure

Author

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  • Jie Ma

    (Beijing Anzhen Hospital of Capital Medical University
    Beijing Institute of Heart Lung and Blood Vessel Diseases)

  • Yang Li

    (Beijing Anzhen Hospital of Capital Medical University
    Beijing Institute of Heart Lung and Blood Vessel Diseases)

  • Ping Li

    (Beijing Anzhen Hospital of Capital Medical University)

  • Xinying Yang

    (Beijing Anzhen Hospital of Capital Medical University
    Beijing Institute of Heart Lung and Blood Vessel Diseases)

  • Shuolin Zhu

    (Beijing Anzhen Hospital of Capital Medical University
    Beijing Institute of Heart Lung and Blood Vessel Diseases)

  • Ke Ma

    (Beijing Anzhen Hospital of Capital Medical University
    Beijing Institute of Heart Lung and Blood Vessel Diseases)

  • Fei Gao

    (Beijing Anzhen Hospital of Capital Medical University)

  • Hai Gao

    (Beijing Anzhen Hospital of Capital Medical University)

  • Hui Zhang

    (Northwestern University)

  • Xin-liang Ma

    (Thomas Jefferson University)

  • Jie Du

    (Beijing Anzhen Hospital of Capital Medical University
    Beijing Institute of Heart Lung and Blood Vessel Diseases)

  • Yulin Li

    (Beijing Anzhen Hospital of Capital Medical University
    Beijing Institute of Heart Lung and Blood Vessel Diseases)

Abstract

Heart failure is the prevalent complication of acute myocardial infarction. We aim to identify a biomarker for heart failure post-acute myocardial infarction. This observational study includes 1062 and 1043 patients with acute myocardial infarction in the discovery and validation cohorts, respectively. The outcomes are in-hospital and long-term heart failure events. S100A8/A9 is screened out through proteomic analysis, and elevated circulating S100A8/A9 is independently associated with heart failure in discovery and validation cohorts. Furthermore, the predictive value of S100A8/A9 is superior to the traditional biomarkers, and the addition of S100A8/A9 improves the risk estimation using traditional risk factors. We finally report causal effect of S100A8/A9 on heart failure in three independent cohorts using Mendelian randomization approach. Here, we show that S100A8/A9 is a predictor and potentially causal medicator for heart failure post-acute myocardial infarction.

Suggested Citation

  • Jie Ma & Yang Li & Ping Li & Xinying Yang & Shuolin Zhu & Ke Ma & Fei Gao & Hai Gao & Hui Zhang & Xin-liang Ma & Jie Du & Yulin Li, 2024. "S100A8/A9 as a prognostic biomarker with causal effects for post-acute myocardial infarction heart failure," Nature Communications, Nature, vol. 15(1), pages 1-13, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-46973-7
    DOI: 10.1038/s41467-024-46973-7
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    References listed on IDEAS

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    1. Amand F. Schmidt & Chris Finan & Maria Gordillo-Marañón & Folkert W. Asselbergs & Daniel F. Freitag & Riyaz S. Patel & Benoît Tyl & Sandesh Chopade & Rupert Faraway & Magdalena Zwierzyna & Aroon D. Hi, 2020. "Genetic drug target validation using Mendelian randomisation," Nature Communications, Nature, vol. 11(1), pages 1-12, December.
    2. Friedman, Jerome H. & Hastie, Trevor & Tibshirani, Rob, 2010. "Regularization Paths for Generalized Linear Models via Coordinate Descent," Journal of Statistical Software, Foundation for Open Access Statistics, vol. 33(i01).
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