Roles of ST2, IL-33 and BNP in predicting major adverse cardiovascular events in acute myocardial infarction after percutaneous coronary intervention

Abstract

This study investigated roles of serum ST2, IL-33 and BNP in predicting major adverse cardiovascular events (MACEs) in acute myocardial infarction (AMI) after percutaneous coronary intervention (PCI). Blood samples were collected from the included AMI patients (n = 180) who underwent PCI. All patients were divided into the MACEs and MACEs-free groups. Enzyme-linked immunosorbent assay was performed to measure serum levels of ST2, IL-33 and BNP. Severity of coronary artery lesion was evaluated by Gensini score. Pearson correlation analysis was used. A receiver operating characteristics curve was drawn to evaluate the potential roles of ST2, IL-33 and BNP in predicting MACEs, and Kaplan-Meier curve to analyse the 1-year overall survival rate. Logistic regression analysis was conducted to analyse the independent risk factors for MACEs. Compared with the MACEs-free group, the serum levels of ST2, IL-33 and BNP were significantly higher in the MACEs group. Serum levels of ST2, IL-33 and BNP were positively correlated with each other and positively correlated with Gensini score. The area under curves of ST2, IL-33 and BNP, respectively, were 0.872, 0.675 and 0.902. The relative sensitivity and specificity were, respectively, 76.27% and 85.92%, 69.49% and 58.68%, as well as, 96.61% and 77.69%. Serum levels of ST2, IL-33 and BNP were independent risk factors for MACEs. The 1-year overall survival rate was higher in AMI patients with lower serum levels of ST2, IL-33 and BNP. In conclusion, serum levels of ST2, IL-33 and BNP have potential value in predicting MACEs in AMI patients undergoing PCI.

Keywords: BNP; Acute myocardial infarction; IL-33; Major adverse cardiovascular events; Percutaneous coronary intervention; ST2.

Figure 1

Comparisons of serum levels of ST2, IL‐33 and BNP in AMI patients at admission between the MACEs and MACEs‐free groups. AMI, acute myocardial infarction; MACEs, major adverse cardiovascular events; ST2, homolog of sulfotransferase; IL‐33, interleukin‐33; BNP, B‐brain natriuretic peptide; *, compared with the MACEs‐free group, P < 0.05.

Figure 2

Correlations of serum levels of ST2, IL‐33 and BNP in AMI patients. AMI, acute myocardial infarction; ST2, homolog of sulfotransferase; IL‐33, interleukin‐33; BNP, B‐brain natriuretic peptide.

Figure 3

Correlations of serum levels of ST2, IL‐33 and BNP with Gensini score in AMI patients. AMI, acute myocardial infarction; ST2, homolog of sulfotransferase; IL‐33, interleukin‐33; BNP, B‐brain natriuretic peptide.

Figure 4

ROC curve analysis on predictive values of serum levels of ST2, IL‐33 and BNP for MACEs. AMI, acute myocardial infarction; ST2, homolog of sulfotransferase; IL‐33, interleukin‐33; BNP, B‐brain natriuretic peptide.

Figure 5

Comparison of the 1‐year overall survival rate in AMI patients between the MACEs and MACEs‐free groups. AMI, acute myocardial infarction; MACE, major adverse cardiovascular events.

Figure 6

Kaplan–Meier curve analysis on the correlations of serum levels of ST2, IL‐33 and BNP with 1‐year overall survival rate in AMI patients. (A) correlations of serum level of ST2 with 1‐year overall survival rate in AMI patients; (B) correlations of serum level of IL‐33 with 1‐year overall survival rate in AMI patients; (C) correlations of serum level of BNP with 1‐year overall survival rate in AMI patients; AMI, acute myocardial infarction; ST2, homolog of sulfotransferase; IL‐33, interleukin‐33; BNP, B‐brain natriuretic peptide.