Identification of Key Genes and Signaling Pathways Involved in Acute Myocardial Infarction and Potential Biomarkers of Its Consequent Heart Failure Based On Bioinformatics Analysis

Backgrounds : Acute myocardial infarction (AMI) is the predominant cause of cardiac death and ischemic heart failure (IHF) worldwide in coronary artery disease (CAD). Although it results from coronary acute occlusion, we in the study explored some key genes involved in the development of AMI and consequent IHF using bioinformatics analysis. Methods Utilizing expression data of 52 patients with AMI and 53 controls from GSE66360 and GSE97320 datasets, we screened shared differentially expressed genes (DEGs) in the independent datasets. Functional enrichment analysis and protein-protein interaction (PPI) network were employed. GSE58967 of 111 AMI patients and 46 controls was used to validate the shared DEGs and further analyzed to identify the DEGs in AMI patients with and without heart failure (HF) with the dynamic changes also being evaluated. The receiver operating characteristic (ROC) curves and area under the curve (AUC) were used to validate the diagnostic efficiency. Results In the comparison of AMI patients with controls, we identified 105 shared DEGs. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis showed the shared DEGs mainly enriched in immune-related inflammation process and pathways. Filtered with PPI network, 5 genes of CXCL8, CXCL1, MMP9, FPR1 and TLR2 were considered as hub genes, which were further validated in GSE59867. Compared with the genes in AMI patients without HF, those of TNFAIP6, ADM, TRIB1, AQP9 and IL1R2 associated with ventricular remodeling were found to be significantly high expressed in patients with HF on admission with the AUC of ROC curves was 0.792–0.847 (all p < 0.05), which can be used as the potential biomarkers for early prediction of HF after AMI. Conclusions These findings based on integrated bioinformatic analysis provide new insights into the important roles of genes to play in the patients with AMI and consequent HF.