Soluble suppression of tumorigenicity 2 (sST2) for predicting disease severity or mortality outcomes in cardiovascular diseases: A systematic review and meta-analysis. (December 2021)

• Record Type: Journal Article
• Authors: Ip, Christina; Luk, King Sum; Yuen, Vincent Lok Cheung; Chiang, Lorraine; Chan, Ching Ki; Ho, Kevin; Gong, Mengqi; Lee, Teddy Tai Loy; Leung, Keith Sai Kit; Roever, Leonardo; Bazoukis, George; Lampropoulos, Konstantinos; Li, Ka Hou Christien; Tse, Gary; Liu, Tong
• Is Part Of: IJC heart & vasculature. Volume 37(2021)
• Publication Date: 2021-12
• Subjects: Soluble suppression of tumorigenicity 2 -- sST2 -- Severity -- Mortality -- Heart failure -- Coronary artery disease; Cardiovascular system -- Diseases -- Periodicals; Cardiovascular system -- Pathophysiology -- Periodicals; 616.1005
• DOI: 10.1016/j.ijcha.2021.100887
• Languages: English
• ISSNs: 2352-9067

Abstract

Abstract: Objectives: Soluble suppression of tumorigenicity 2 (sST2) is a member of the interleukin-1 receptor family. It is raised in various cardiovascular diseases, but its value in predicting disease severity or mortality outcomes has been controversial. Therefore, we conducted a systematic review and meta -analysis to determine whether sST2 levels differed between survivors and non-survivors of patients with cardiovascular diseases, and whether elevated sST2 levels correlated with adverse outcomes. Methods: PubMed and Embase were searched until 23rd June 2021 for studies that evaluated the relationship between sST2 levels and cardiovascular disease severity or mortality. Results: A total of 707 entries were retrieved from both databases, of which 14 studies were included in the final meta -analysis. In acute heart failure, sST2 levels did not differ between survivors and non-survivors (mean difference [MD]: 24.2 ± 13.0 ng/ml; P = 0.06; I 2 : 95%). Elevated sST2 levels tend to be associated with increased mortality risk (hazard ratio [HR]: 1.12, 95 %CI: 0.99–1.27, P = 0.07; I 2 : 88%). In chronic heart failure, sST2 levels were higher in non-survivors than in survivors (MD: 0.19 ± 0.04 ng/ml; P = 0.001; I 2 : 0%) and elevated levels were associated with increased mortality risk (HR: 1.64, 95% CI: 1.27–2.12, P < 0.001; I 2 : 82%). sST2 levels were significantly higher in severe disease compared to less severe disease (MD: 1.56 ± 0.46 ng/ml; P = 0.001; I 2 : 98%). Finally, in stable coronary artery disease, sST2 levels were higher in non-survivors than survivors (MD: 3.0 ± 1.1 ng/ml; P = 0.005; I 2 : 80%) and elevated levels were significantly associated with increased mortality risk (HR: 1.32, 95% CI: 1.04–1.68, P < 0.05; I 2 : 57%). Conclusions: sST2 significantly predicts disease severity and mortality in cardiovascular disease and is a good predictor of mortality in patients with stable coronary artery disease and chronic heart failure.