Background Ischemic cardiomyopathy (ICM) with high morbidity and mortality is closely associated with an abnormal equilibrium of circulation selenium levels. The oxidative stress theory is the most accepted theory of selenium causing ischemic cardiomyopathy. However, the role of inflammatory responses in ICM has received limited attention. Methods This study included 119 subjects, 43 of whom were patients with ICM, and 76 were healthy controls. Blood specimens were collected from subjects and serum levels of inflammatory and oxidative stress indicators and plasma levels of selenium were measured. Results When plasma selenium and indicators of inflammation and oxidative stress were compared between groups, plasma selenium levels were significantly lower in the ICM group than in the control group (68.83874 vs 104.39775, p =0.02032), while indicators of inflammation such as tumour necrosis factor-alpha (TNF-α) (79.09773 vs 46.15634, p <0.001), interleukin-6 (IL-6) (49.41484 vs 38.46923, p <0.01) and neutrophil/lymphocyte ratio (3.696574 vs 2.383658, p <0.001) were significantly higher in the ICM group than in the control group (all of these results were statistically different). Additionally, malondialdehyde (MDA), a marker of oxidative stress, was considerably higher in the ICM group than in the control group (61.63078 vs 39.0609, p <0.01). In contrast, there were no significant differences in superoxide dismutase (SOD) levels between groups ( p >0.05). The Poisson regression analysis revealed a significant association between selenium and high levels of MDA, IL-6 and TNF-α ( p <0.05). Additionally, selenium was negatively connected with SOD levels and the neutrophil/lymphocyte ratio, but this relationship was not statistically significant ( p =0.96, 0.15, respectively). Conclusion Selenium deficiency is strongly associated with the development of ICM, and with levels of inflammation and oxidative stress in patients with ICM. Selenium can prevent the development and delay the progression of ICM by alleviating inflammatory responses.

Background: Ischemic cardiomyopathy (ICM) with high mobility and mortality is closely linked to immunology, oxidative stress, inflammatory response and so on. Early diagnosis counts for the effective treatment of ICM. However, there are still no distinctive diagnostic signatures. This research aims to investigate effective signatures and build the diagnostic model for ICM. Methods: The Gene Expression Omnibus was used to retrieve the microarray data of GSE9800 and GSE580, which were obtained from tissue biopsy samples. Differentially expressed genes (DEGs), GO, and KEGG analyses were then carried out on the microarray data. The PPI network was constructed via STRING database.Following that, CIBERSORT techniques in conjunction with the LM22 feature matrix were used to assess the immune infiltration of the samples.The expression of a few chosen genes served as the predictor variable, and the occurrence of ICM served as the responder variable, in the construction of the best subset stepwise regression model. Results: A total of 28 DEGs were found. And according to the GO and KEGG studies, numerous biological processes were enriched. Patients with ICM and their normal counterparts had considerably distinct immune cell types infiltrating. For the construction of the PPI network, the top 20 most significant DEGs were selected and were used to build the original regression model. The optimal subset screened using stepwise regression analysis contained three pivotal genes (SCD, SNX25, WNT7B) and the area under the curve (AUC) values in this model was 0.891. Conclusion:We identified several possible hub genes, including SCD, SNX25, and WNT7B, which may be strongly related to the development of ICM. Based on the three genes, the logistic regression model could be used to accurately diagnose ICM patients.