Association between soluble suppression of tumorigenicity 2 and risk and severity of coronary artery disease: a case control study.

BACKGROUND

To investigate the differential expression of soluble suppression of tumorigenicity 2 (sST2) in patients with coronary artery disease (CAD) and healthy controls, and the correlation between sST2 and the severity of coronary artery atherosclerosis.

METHODS

A total of 911 CAD patients were selected as the CAD group, and 322 healthy people were selected as the control group. We measured serum sST2 level by chemiluminescence immunoassay, and applied the Gensini scoring system to quantify the severity of coronary artery atherosclerosis. We utilized Mann-Whitney U test to assess the difference of sST2 level between the two groups, and adopted Spearman correlation test to evaluate the correlation between sST2 level and Gensini score and inflammatory indexes.

RESULTS

Compared with the control group, the expression level of sST2 in CAD group was significantly increased [29.20 (20.67, 46.34) vs. 19.69 (15.97, 25.02), P < 0.001]. Logistic regression showed that sST2 expression could increase CAD risk (OR = 1.099, 95%CI: 1.080 ~ 1.119, P < 0.001). Analysis of variance revealed that the sST2 expression level increased gradually in unstable angina pectoris group (UA), non-ST elevation myocardial infarction group (NSTEMI) and ST elevation myocardial infarction group (STEMI) [UA: 23.05 (17.54, 30.75), NSTEMI: 30.71 (21.31, 42.97), STEMI: 51.05 (32.85, 80.04), P < 0.001]. Spearman correlation analysis demonstrated significantly positive associations between sST2 expression level and Gensini score (r = 0.137, P < 0.001), and systemic inflammatory indexes MHR (r = 0.188, P < 0.001), NLR (r = 0.469, P < 0.001), PLR (r = 0.285, P < 0.001) and MLR (r = 0.368, P < 0.001), but negatively correlated with AFR (r=-0.135, P < 0.001). By receiver operating characteristic (ROC) curve analysis, the sST2 expression level had excellent predictive effect in STEMI with the area under the curve (AUC) value of 0.926 (95%CI: 0.903-0.948, P < 0.001) and sensitivity and specificity of 72.3% and 99.7% respectively, superior to NSTEMI with an AUC of 0.760 (95%CI: 0.719-0.802, P < 0.001) and UA with an AUC of 0.616 (95%CI: 0.576-0.656, P < 0.001).

CONCLUSIONS

sST2 could not only serve as a biomarker for the clinical auxiliary diagnosis of CAD, but also act as a potential indicator for disease progression or risk stratification. Dynamic monitoring of sST2 levels might assist in evaluating treatment efficacy.