Abstract

BackgroundThymic stromal lymphopoietin (TSLP), a distant paralog of the cytokine IL-7, has been shown to be associated with atherosclerosis. However, the effect of plasma TSLP level after acute myocardial infarction (AMI) remains largely unclear. Thus, we aimed to assess the relationship between the concentration of TSLP at admission and the risk of major adverse cardiovascular events (MACE) in AMI patients.MethodsA total of 175 patients with AMI and 145 unstable angina (UA) controls were recruited in the present study. The clinical characteristics were collected, and MACE was recorded during hospitalization and the follow-up period after discharge.ResultsThe median value (25, 75 percentiles) of TSLP concentrations in the AMI group was higher than that in the UA group [11.18 (8.14–15.22) vs. 8.56 (5.26–11.94) pg/ml, p < 0.001, respectively]. Multivariate linear regression analysis revealed that Troponin-I (standardized β = 0.183, p = 0.004) was an independent factor for TSLP. According to the median of TSLP concentrations, all the AMI patients were divided into the high-level group (TSLP level ≥ 11.18 pg/ml, N = 91) and the low-level group (TSLP <11.18 pg/ml, N = 84). In a receiver operating characteristic curve analysis, the area under the curve for TSLP as a predictor of AMI was 0.674 with a cut-off value of 9.235 pg/ml. After a median follow-up of 14 months, Kaplan-Meier survival analysis showed no significant difference in MACE-free survival between the two groups (p = 0.648). Finally, the multivariate logistic regression analyses demonstrated that TSLP was a negative predictor of MACE in AMI patients (OR:0.778,95% CI:0.733–0.876, p = 0.032).ConclusionsPlasma TSLP levels were elevated in patients with AMI than those in UA. The lower TSLP concentration was associated with MACE after AMI.

Highlights

  • Coronary artery disease (CAD) has emerged as a common cause of death over the past few decades

  • The multivariate logistic regression analyses demonstrated that Thymic stromal lymphopoietin (TSLP) was a negative predictor of major adverse cardiovascular events (MACE) in Acute myocardial infarction (AMI) patients (OR:0.778,95% CI:0.733–0.876, p = 0.032)

  • Plasma TSLP levels were elevated in patients with AMI than those in unstable angina (UA)

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Summary

Introduction

Coronary artery disease (CAD) has emerged as a common cause of death over the past few decades. TSLP is associated with the pathogenesis of type 2 inflammatory diseases, such as asthma, atopic dermatitis, and inflammatory bowel disease [4–6]. These diseases are often complicated by thrombotic events [7–9]. Yu et al found that TSLP was nearly undetectable in cardiovascular tissue of apolipoprotein E-deficient (ApoE–/–) mice. They found that mice treated with TSLP had significantly fewer atherosclerotic plaques compared with controls, suggesting that TSLP attenuates the development of atherosclerosis [11]. The effect of plasma TSLP level after acute myocardial infarction (AMI) remains largely unclear. We aimed to assess the relationship between the concentration of TSLP at admission and the risk of major adverse cardiovascular events (MACE) in AMI patients

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