Key result
Dysregulated S100A12 transcription is linked to ~4.6-fold higher mortality after STEMI.
Why the study?
The ability of blood transcriptome analysis to identify dysregulated pathways and outcome-related genes following myocardial infarction remains unknown.
Observational (n=223)
Hazard Ratio: 4.621 (95% CI 1.135–18.816)
p-value: p=0.033
Dysregulated expression of plasma S100A12 at the transcriptional level is a robust early prognostic factor in STEMI patients, though its protein level requires further validation.
May warrant transcriptional S100A12 assessment for STEMI prognostication; leaves open protein-level validation and therapeutic implications.
The ability of blood transcriptome analysis to identify dysregulated pathways and outcome-related genes following myocardial infarction remains unknown. Two gene expression datasets (GSE60993 and GSE61144) were downloaded from Gene Expression Omnibus (GEO) Datasets to identify altered plasma transcriptomes in patients with ST-segment elevated myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention. GEO2R, Gene Ontology/Kyoto Encyclopedia of Genes and Genomes annotations, protein-protein interaction analysis, etc., were adopted to determine functional roles and regulatory networks of differentially expressed genes (DEGs). Dysregulated expressomes were verified at transcriptional and translational levels by analyzing the GSE49925 dataset and our own samples, respectively. A total of 91 DEGs were identified in the discovery phase, consisting of 15 downregulated genes and 76 upregulated genes. Two hub modules consisting of 12 hub genes were identified. In the verification phase, six of the 12 hub genes exhibited the same variation patterns at the transcriptional level in the GSE49925 dataset. Among them, S100A12 was shown to have the best discriminative performance for predicting in-hospital mortality and to be the only independent predictor of death during follow-up. Validation of 223 samples from our center showed that S100A12 protein level in plasma was significantly lower among patients who survived to discharge, but it was not an independent predictor of survival to discharge or recurrent major adverse cardiovascular events after discharge. In conclusion, the dysregulated expression of plasma S100A12 at the transcriptional level is a robust early prognostic factor in patients with STEMI, while the discrimination power of the protein level in plasma needs to be further verified by large-scale, prospective, international, multicenter studies.
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Zhai et al. (2022) conducted an observational in ST-Segment Elevated Myocardial Infarction (STEMI) (n=223). S100A12 expression vs. Lower S100A12 expression was evaluated on Death during follow-up (transcriptional level) (HR 4.621, 95% CI 1.135-18.816, p=0.033). Dysregulated expression of plasma S100A12 at the transcriptional level was an independent predictor of death during follow-up in STEMI patients (HR 4.621), although plasma protein levels were not an independent predictor of survival or recurrent MACE.
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