Preliminary study of beta-blocker therapy on modulation of interleukin-33/ST2 signaling during ventricular remodeling after acute myocardial infarction

Xia, Jinggang; Qu, Yang; Yin, Chunlin; Xu, Dong

doi:10.5603/cj.a2016.0096

Cited by 14 publications

(10 citation statements)

References 25 publications

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“…There are several studies showing the potential advantageous influence of renin -angiotensin -aldosterone antagonists, as well as genetic therapies on the reduction of biomarker levels. [34][35][36][37][38] Other mediators of inflammatory processes (ie, leukotrienes) have recently been pathophysiological pathways than that which are already known. AMI provokes an inflammatory response with the migration of a multitude of cells and regulators into the infarcted and noninfarcted areas.…”

Section: Discussionmentioning

confidence: 99%

Association of galectin-3 and soluble ST2 with in-hospital and one-year outcomes in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention

Tymińska¹,

Kapłon‐Cieślicka²,

Ozierański³

et al. 2019

Polish Archives of Internal Medicine

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INTRODUCTION Galectin-3 (Gal-3) and soluble interleukin-1 receptor-like 1 (sST2) have known prognostic value in already diagnosed heart failure (HF). OBJECTIVES To investigate the association of Gal-3 and sST2 with prognosis in patients with ST-segment elevation myocardial infarction (STEMI) treated with primary percutaneous coronary intervention (pPCI). PATIENTS AND METHODS The analysis was based on data collected in a prospective observational BIOSTRAT (Biomarkers for Risk Stratification After STEMI; ClinicalTrials.gov identifier, NCT03735719) study. Analysis included 117 patients with first-time STEMI treated with pPCI. Serum for Gal-3 and sST2 was sampled 72 to 96 hours after admission due to STEMI. The patients were followed for the primary endpoint (cardiovascular [CV] death or HF hospitalization at 1 year). RESULTS Both biomarkers correlated with N-terminal pro-B-type natriuretic peptide (NT-proBNP); Gal-3 correlated with older age. Data on the primary endpoint were available for 104 patients (89%). At 1-year follow-up, 9 patients (8.7%) reached the primary endpoint. In univariate Cox proportional hazards regression analysis, both Gal-3 and sST2 as continuous variables, as well as their newly-established cut offs (≥9.57 ng/ml for Gal-3 and ≥45.99 ng/ml for sST2, based on the Youden index) were predictors of the primary endpoint, and of HF hospitalizations alone. Gal-3 also predicted CV death. After adjustment for age and NT-proBNP, Gal-3 and sST2 remained predictors of the primary endpoint in multivariate models. CONCLUSIONS In patients with first-time STEMI treated with pPCI, baseline Gal-3 and sST2 predicted the composite of CV death and HF hospitalization at 1 year. Both biomarkers may play an important role in CV risk stratification after STEMI, although Gal-3 may be considered preferable.

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Section: Discussionmentioning

confidence: 99%

Association of galectin-3 and soluble ST2 with in-hospital and one-year outcomes in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention

Tymińska¹,

Kapłon‐Cieślicka²,

Ozierański³

et al. 2019

Polish Archives of Internal Medicine

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“…Comparison of MCS patients with HF patients in this study showed that these two patient groups in part required modification in pharmacologic therapy due to LVAD implantation, e.g., more antiplatelet drugs, PDE5i and calcium antagonists but less antiarrhythmic therapy. Here, medication may additionally affect local signaling, since several studies report the influence of these agents on IL-1 signaling [ 33 , 34 ]) or IL-33 signaling [ 35 , 36 ]. Our study provides insight into the topographic differences between the LV and RV myocardia.…”

Section: Discussionmentioning

confidence: 99%

Altered mRNA Expression of Interleukin-1 Receptors in Myocardial Tissue of Patients with Left Ventricular Assist Device Support

Niazy

Mrozek

Barth

et al. 2021

JCM

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Serum levels of cytokines interleukin 1 beta (IL-1β) and interleukin 33 (IL-33) are highly abnormal in heart failure and remain elevated after mechanical circulatory support (MCS). However, local cytokine signaling induction remains elusive. Left (LV) and right ventricular (RV) myocardial tissue specimens of end-stage heart failure (HF) patients without (n = 24) and with MCS (n = 39; 594 ± 57 days) were analyzed for cytokine mRNA expression level of IL-1B, interleukin 1 receptor 1/2 (IL-1R1/2), interleukin 1 receptor-like 1 (IL-1RL1), IL-33 and interleukin-1 receptor accessory protein (IL-1RaP). MCS patients showed significantly elevated IL-1B expression levels (LV: 2.0 fold, p = 0.0058; RV: 3.3 fold, p < 0.0001). Moreover, IL-1R1, IL-1RaP and IL-33 expression levels strongly correlated with each other. IL-1RL1 and IL-1R2 expression levels were significantly higher in RV myocardial tissue (RV/LV ratio IL-1R2 HF: 4.400 ± 1.359; MCS: 4.657 ± 0.655; IL-1RL1 HF: 3.697 ± 0.876; MCS: 4.529 ± 0.5839). In addition, IL1-RaP and IL-33 RV expression levels were significantly elevated in MCS. Furthermore, IL-33 expression correlates with C-reactive protein (CRP) plasma levels in HF, but not in MCS patients. Increased expression of IL-1B and altered correlation patterns of IL-1 receptors indicate enhanced IL-1β signaling in MCS patients. Correlation of IL-1 receptor expression with IL-33 may hint towards a link between both pathways. Moreover, diverging expression in LV and RV suggests specific regulation of local cytokine signaling.

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“…IL-33 improved cardiac function after MI through ST2 signalling. 35 Shimpo et al speculated that once AMI happened the remaining viable myocardium had to bear great stress, when sST2 was induced in mechanically overloaded cardiac myocytes and released into the circulation in patients. 26 Therefore, we speculated that the increased release of sST2 weakened the cardioprotective effects of IL-33/ST2L pathway, which might be associated with lack of myocardial reperfusion.…”

Section: Discussionmentioning

confidence: 99%

Predictive value of soluble suppression of tumourigenicity 2 on myocardial reperfusion

Bai

Liu

et al. 2020

Internal Medicine Journal

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Background High baseline level of soluble suppression of tumourigenicity 2 (sST2) was an independent predictor of cardiovascular death and heart failure in ST‐segment elevation myocardial infarction (STEMI). Aims To investigate the value of serum sST2 baseline levels in predicting myocardial reperfusion in patients with STEMI undergoing primary percutaneous coronary intervention (PPCI). Methods Consecutive STEMI patients who underwent PPCI within 12 h after the onset of chest pain were enrolled, and were divided into Thrombolysis In Myocardial Infarction (TIMI) myocardial perfusion grading (TMPG) 0/1/2 group and TMPG 3 group based on post‐procedural TMPG. Baseline clinical characteristics, lesions and procedural characteristics were compared. Univariate logistic regression and multivariate linear logistic analysis were performed to identify independent predictors of impaired myocardial reperfusion (TMPG 0/1/2). Receiver‐operating characteristics curve (ROC) analysis of sST2 was performed to identify the optimum cut‐off value for predicting the myocardial reperfusion. Results A total of 121 patients was enrolled in this study. Univariate logistic regression analysis showed that Killip II–III, high levels of sST2 and brain natriuretic peptide were risk factors of TMPG 0/1/2. Multivariable logistic regression analysis revealed that sST2 was an independent predictor of impaired myocardial reperfusion (odds ratio 12.318, 95% confidence interval 4.567–33.220, P < 0.001). ROC curve analysis showed that the area under curve of sST2 was 0.849, and the best cut‐off value was 2.003 ng/mL, with a sensitivity of 89.2% and a specificity of 67.9%. Conclusion The elevated levels of sST2 on admission were associated with impaired myocardial reperfusion in STEMI patients undergoing PPCI.

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Preliminary study of beta-blocker therapy on modulation of interleukin-33/ST2 signaling during ventricular remodeling after acute myocardial infarction

Abstract: (Cardiol J 2017; 24, 2: 188-194)

Cited by 14 publications

References 25 publications

Association of galectin-3 and soluble ST2 with in-hospital and one-year outcomes in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention

Association of galectin-3 and soluble ST2 with in-hospital and one-year outcomes in patients with ST-segment elevation myocardial infarction treated with primary percutaneous coronary intervention

Altered mRNA Expression of Interleukin-1 Receptors in Myocardial Tissue of Patients with Left Ventricular Assist Device Support

Predictive value of soluble suppression of tumourigenicity 2 on myocardial reperfusion

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