Soluble Suppression Of Tumorigenicity Research Articles

Role of Cardiac Biomarkers in Hepatic Disorders: A Literature Review.

Various studies have reported the association between cardiac markers and hepatic disorders. The main objective of this review article was to elucidate the significance of important cardiac indicators such as ischemia-modified albumin, cardiac troponin, cardiac natriuretic peptides, creatine kinase, creatine kinase-MB, lactate dehydrogenase, heart-type fatty acid-binding protein, osteopontin, soluble suppression of tumorigenicity 2, C-reactive protein, and lipoprotein(a) in the development of hepatic disorders. In addition, it highlighted recent notable discoveries and accomplishments in this field and identified areas requiring further investigation, ongoing discussions, and potential avenues for future research. Early identification and control of these cardiac markers might be helpful to control the prevalence of hepatic disorders associated with cardiovascular diseases.

Prognostic value of morphological, biochemical, molecular markers of fibrosis in patients with hypertrophic cardiomyopathy

Hypertrophic cardiomyopathy (HCM) at the cellular level is characterized by hypertrophy, cardiomyocyte disorganization and myocardial fibrosis areas. The leading death cause in HCM remains sudden cardiac death (SCD). Despite the existing risk scores for SCD in HCM, there are still patients with uncertain SCD risk. In addition, SCD cases are also recorded among low-risk patients. From the above, search for novel markers for a more accurate risk assessment should be continued. Fibrosis is currently suspected to be a substrate of potentially life-threatening ventricular arrhythmias. Despite the increasingly widespread use of cardiac magnetic resonance imaging in the diagnosis of myocardial fibrosis and stratification of patients at high SCD risk, the determination of myocardial fibrosis biomarkers remains a relevant and promising area. The article presents the results of studies proving the diagnostic significance and relationship with the risk of life-threatening cardiac arrhythmias of the following markers: C-propeptide of type I procollagen, matrix metalloproteinase proteins, tissue inhibitor of metalloproteinases 1, microRNA family, soluble suppression of tumorigenicity 2, galectin-3, apelin. Evaluation of these biomarkers can be used to improve risk stratification of patients with HCM.

Novel Biomarkers in Early Detection of Heart Failure: A Narrative Review.

Heart failure (HF) represents a significant global health challenge, characterized by a variety of symptoms resulting from cardiac dysfunction. This dysfunction often leads to systemic and pulmonary congestion. The pathophysiology of HF is complex, involving stimulation of the sympathetic nervous system, which is insufficiently balanced by the release of natriuretic peptide. This imbalance leads to progressive hypertrophy and dilatation of the heart's chambers, impairing its pumping efficiency and increasing the risk of arrhythmias and conduction disorders. The prevalence of HF is exceptionally high in industrialized nations and is expected to increase owing to an aging population and advancements in diagnostic methods. This study emphasizes the critical role of early diagnosis in reducing morbidity and mortality associated with HF, focusing specifically on the evolving importance of biomarkers in managing this condition. Biomarkers have played a key role in transforming the diagnosis and treatment of HF. Traditional biomarkers such as b-type natriuretic peptide and N-terminal pro-b-type natriuretic peptide have been widely adopted for their cost-effectiveness and ease of access. However, the rise of novel biomarkers such as growth differentiation factor 15 and adrenomedullin has shown promising results, offering superior sensitivity and specificity. These new biomarkers enhance diagnostic accuracy, risk stratification, and prognostic evaluation in HF patients. Despite these advancements, challenges remain, such as limited availability, high costs, and the need for further validation in diverse patient populations. Through a comprehensive literature review across databases such as PubMed, Google Scholar, and the Cochrane Library, this study compiles and analyzes data from 18 relevant studies, offering a detailed understanding of the current state of HF biomarkers.The study examines both traditional and emerging biomarkers such as galectin-3 and soluble suppression of tumorigenicity 2 in HF, exploring their clinical roles and impact on patient outcomes.

Heart transplantation and biomarkers: a review about their usefulness in clinical practice.

Advanced heart failure (AdvHF) can only be treated definitively by heart transplantation (HTx), yet problems such right ventricle dysfunction (RVD), rejection, cardiac allograft vasculopathy (CAV), and primary graft dysfunction (PGD) are linked to a poor prognosis. As a result, numerous biomarkers have been investigated in an effort to identify and prevent certain diseases sooner. We looked at both established biomarkers, such as NT-proBNP, hs-troponins, and pro-inflammatory cytokines, and newer ones, such as extracellular vesicles (EVs), donor specific antibodies (DSA), gene expression profile (GEP), donor-derived cell free DNA (dd-cfDNA), microRNA (miRNA), and soluble suppression of tumorigenicity 2 (sST2). These biomarkers are typically linked to complications from HTX. We also highlight the relationships between each biomarker and one or more problems, as well as their applicability in routine clinical practice.

Relationship between serum soluble suppression of tumorigenicity (ST) 2 and global longitudinal strain in early onset preeclampsia

BackgroundPreeclampsia is one of the leading causes of death in childbearing women worldwide. Hemodynamic changes in preeclampsia can trigger cardiac remodeling as indicated by increase of soluble-ST2 (sST2). Global longitudinal strain were able to detect systolic dysfunction better than the ejection fraction. This study aims to evaluate the correlation between serum levels of sST2 towards GLS in patients with early-onset preeclampsia.MethodsThis is a cross-sectional observational study with correlation analysis. Subjects were patients with severe preeclampsia with gestational age before 34 weeks at Dr. Hasan Sadikin Central General Hospital Bandung and Bandung Kiwari Regional General Hospital from June to August 2022. Examination of sST2 was carried out through blood samples using the ELISA method. sST2 was measured using Presage ST2 Assay reagent. GLS examination was carried out using speckle tracking technique with EchoPAC. Correlation analysis was conducted using the Pearson test if normally distributed, otherwise Spearman’s correlation was conducted. Correlation analysis was followed by linear regression.ResultsA total of 30 patients met the inclusion criteria. The mean age was 30.83 ± 7.09, with 17 (56.7%) multiparous patients. The median sST2 was 145.75 ng/mL, and the median GLS was − 17.4%. Spearman correlation analysis showed that there was a significant positive correlation with moderate strength between sST2 and GLS (r = 0.583; p < 0.002). Linear regression showed that every 1 ng/ml increase in sST2 would give an increase in GLS of 0.014%.ConclusionThere is a significant correlation between sST2 and GLS in patients with early onset severe preeclampsia.

Soluble suppression of tumorigenicity 2 associated with major adverse cardiac events in children with myocarditis.

Soluble suppression of tumorigenicity 2 (sST2) is associated with the prognosis of some cardiac diseases, but studies on sST2 and the prognosis of patients with myocarditis are rare. This study investigated the relationship between major adverse cardiovascular events (MACEs) and sST2 during hospitalization in pediatric patients with myocarditis. This was a single-center retrospective cohort study. A total of 252 patients aged ≤14 years diagnosed with myocarditis were enrolled. Events during the hospitalization were defined as MACEs (all-cause death > new heart failure > ventricular arrhythmia). A total of 25 people had MACEs during their hospital stay. The mortality during hospitalization was 6/23 (26%) in patients with heart failure and 3/10 (30%) in patients with ventricular arrhythmias. After including these risk factors in a multivariate logistic regression analysis, NT-proBNP (OR 4.323; 95% CI, 2.433-7.679; p < 0.001) and sST2 (OR 1.020; 95% CI, 1.003-1.037; p = 0.022) remained statistically significant and were independent risk factors for MACEs during hospitalization in pediatric myocarditis patients. Elevated levels of NT-proBNP and sST2 were independently associated with major adverse cardiovascular events during hospitalization in children with myocarditis, and both showed good predictive efficacy.

Иммунные механизмы нейтрофильного воспаления при бронхиальной астме

This review presents an analysis of scientific publications in recent years devoted to the study of cellular and molecular mechanisms of neutrophilic airway inflammation as potential therapeutic targets in the treatment of severe, poorly controlled asthma of the neutrophil phenotype, the presence of which is still debated and there is no generally accepted definition. The conditional term "neutrophilic asthma" implies the existence of a certain asthma endotype, in which neutrophils are the main type of cells mediating the pathophysiology and disease symptoms. The involvement of the inverted protein response associated with endoplasmic reticulum (ER) stress and the sensory signal transduction protein in the endoplasmic reticulum membrane in the deregulation of the T helper 17 (Th17) cells function and neutrophilic airway inflammation is considered. Polarization and activation of M1 macrophages play an important role in the neutrophilic inflammation immunopathogenesis, in particular, in asthma associated with obesity. Soluble suppression of tumorigenicity 2 protein is considered as a receptor that promotes neutrophil activation and neutrophilic inflammation. The involvement of neutrophil extracellular traps and the respiratory tract microbiome in the neutrophilic inflammation progression, in particular, the role of bacterial outer membrane vesicles, is discussed. KEYWORDS: neutrophils, neutrophilic inflammation, asthma, Th17 cells, M1 macrophages, suppression of tumorigenicity 2 protein, neutrophil extracellular traps, respiratory tract microbiome. FOR CITATION: Kuzubova N.A., Lebedeva E.S. Immune mechanisms of neutrophilic inflammation in asthma. Russian Medical Inquiry. 2024;8(8):453–458 (in Russ.). DOI: 10.32364/2587-6821-2024-8-8-2.

ST2-Mediated Neutrophilic Airway Inflammation: A Therapeutic Target for Patients With Uncontrolled Asthma.

Suppression of tumorigenicity 2 (ST2) has been proposed as the receptor contributing to neutrophilic inflammation in patients with type 2-low asthma. However, the exact role of ST2 in neutrophil activation remains poorly understood. A total of 105 asthmatic patients (classified into 3 groups according to control status: the controlled asthma [CA], partly-controlled asthma [PA], and uncontrolled asthma [UA] groups), and 104 healthy controls were enrolled to compare serum levels of soluble ST2 (sST2) and interleukin (IL)-33. Moreover, the functions of ST2 in neutrophils and macrophages (Mϕ) were evaluated ex vivo and in vivo. Serum sST2 levels were significantly higher in the UA group than in the CA or PA groups (P < 0.05 for all) with a negative correlation between serum sST2 and forced expiratory volume in 1 second % (r = -0.203, P = 0.038). Significantly higher expression of ST2 receptors on peripheral neutrophils was noted in the UA group than in the PA or CA groups. IL-33 exerted its effects on the production of reactive oxygen species, the formation of extracellular traps from neutrophils, and Mϕ polarization/activation. In neutrophilic asthmatic mice, treatment with anti-ST2 antibody significantly suppressed proinflammatory cytokines (tumor necrosis factor-alpha and IL-17A) as well as the numbers of immune cells (neutrophils, Mϕ, and group 3 innate lymphoid cells) in the lungs. These results suggest that IL-33 induces the activation of neutrophils and Mϕ via ST2 receptors, leading to neutrophilic airway inflammation and poor control status of asthma. ST2 could be a therapeutic target for neutrophilic airway inflammation in patients with UA.

Chronic Kidney Disease Associated with Ischemic Heart Disease: To What Extent Do Biomarkers Help?

Chronic kidney disease represents a complex and multifaceted pathology characterized by the presence of structural or functional renal anomalies associated with a persistent reduction in renal function. As the disease progresses, complications arise due to the chronic inflammatory syndrome, hydro-electrolytic disorders, and toxicity secondary to the uremic environment. Cardiovascular complications are the leading cause of death for these patients. Ischemic cardiac pathology can be both a consequence and complication of chronic kidney disease, highlighting the need to identify specific cardiorenal dysfunction biomarkers targeting pathophysiological mechanisms common to both conditions. This identification is crucial for establishing accurate diagnoses, prognoses, and risk stratifications for patients. This work is intended to elucidate the intricate relationship between chronic kidney disease and ischemic heart disease and to investigate the roles of cardiorenal biomarkers, including cardiac troponin, natriuretic peptides, galectin-3, copeptin, fibroblast growth factor 23 and its co-receptor Klotho, soluble suppression of tumorigenicity 2, and plasma growth differentiation factor 15.

Interleukin 33, soluble suppression of tumorigenicity 2, interleukin 27, and galectin 3 as predictors for outcome in patients admitted to intensive care units.

Intensive care units (ICUs) are expert hospital areas that provide treatment and 24 h care for people who are very sick. Sepsis represents a serious, severe condition and it can lead to septic shock and multiple organ dysfunction syndromes and is one of the most common reasons for patients' hospitalization in ICUs. We wanted to explore the prognostic values of interleukin (IL) 33, soluble suppression of tumorigenicity 2 (sST2), IL 27, and galectin 3 in critically-ill patients. We assumed that these parameters in combination or alone could predict mortality in ICU patients. This research represents a clinical non-randomized prospective study, performed at the Medical Military Academy, a tertiary care hospital in Belgrade, Serbia. The patients were divided in four groups: patients with sepsis (peritonitis, pancreatitis, trauma) and patients without sepsis (trauma). Total number of patients enrolled in the study was 151 and average years of patients were 56.48. The values greater than the cut-off were the predictors of mortality. The IL-33, IL-27 as well as galectin-3 can successfully predict the outcome of critically-ill patients in ICUs. The sST2, cannot predict death in critically-ill patients as a single prognostic factor. However, the combination of at least two biomarkers: IL-33, sST2, IL-27, and galectin-3, gives very significant results in predicting the outcome in patients admitted to ICUs.

Soluble Suppression of Tumorigenicity 2 (sST2) in Patients with Predominantly Decompensated Right Heart Failure—A Prospective Observational Study

Right heart failure is a major challenge in clinical practice. Soluble Suppression of Tumorigenicity-2 (sST2), a member of the interleukin-1-receptor family, may have clinical prognostic value. The aim of this study was to analyze whether sST2 correlates with signs of acute right heart decompensation. This prospective single-center study included 50 patients admitted for clinical signs of predominant right heart decompensation. Signs of reduced blood supply to other organs (e.g., renal function parameter, troponin T, NT-proBNP), diuretics, and signs of venous congestion (inferior vena cava (IVC) diameter) with fluid retention (weight gain, peripheral edema) resulting from reduced RV function were analyzed. The degree of peripheral edema was defined as none, mild (5–6 mm depressible, regression in 15–60 s) or severe (&gt;7 mm depressible, regression in 2–3 min). sST2 levels were measured at the day of hospitalization. A total of 78.7% showed severe peripheral edema. The median concentration of sST2 was 35.2 ng/mL (25.–75. percentiles 17.2–46.7). sST2 is correlated with the peripheral edema degree (rSpearman = 0.427, p = 0.004) and the diameter of IVC (r = 0.786, p = 0.036), while NT-proBNP (r = 0.114, p = 0.456), troponin T (r = 0.123, p = 0.430), creatinine-based eGFR (r = −0.207, p = 0.195), or cystatin C-based eGFR (r = −0.032, p = 0.839) did not. sST2, but no other established marker, is correlated with peripheral and central fluid status in patients with decompensated right heart failure.

Inflammation in acute heart failure.

Acute heart failure (AHF) represents a common clinical scenario that requires prompt evaluation and therapy and that is characterized by a high risk of mortality or subsequent rehospitalizations. The pathophysiology leading to AHF decompensation is still not fully understood. Significant activation of inflammatory pathways has been identified in patients with AHF, particularly in its most severe forms, and it has been hypothesized that systemic inflammation has a role in AHF pathogenesis. Several inflammatory mediators and cytokines, such as high sensitivity C-reactive protein, tumor necrosis factor-α, interleukin-6, interleukin-1, soluble suppression of tumorigenicity 2 and galectin-3, have been shown to play a role in the pathogenesis, development and worsening of this condition with an independent prediction of adverse outcomes. This manuscript reviews the prevalence and prognostic value of systemic inflammation in AHF, as well as the potential role of anti-inflammatory therapies, focusing on available evidence from clinical trials and ongoing studies.

Blood biomarkers to detect functional impairment in adult patients with repaired tetralogy of Fallot

BackgroundThe relationship between plasma brain natriuretic peptide (NT-proBNP) and soluble suppression of tumorigenicity-2 (sST2) with structural adaptions and exercise capacity remains incompletely described in patients with repaired Tetralogy of Fallot (rTOF). MethodsPeripheral venous blood samples were drawn for 99 patients with repaired TOF, 59 patients with severe pulmonary regurgitation (PR) and 40 patients with no or mild PR. NT-proBNP was measured using enzyme-linked immunosorbent assays (Roche Diagnostics, Indianapolis, IN). Soluble ST2 levels were assessed on Aspect-plus ST2 quantitative rapid test. ResultsThe mean value of NT-proBNP was 160 ± 137 pg/ml, and sST2 was 29 ± 13, ng/ml in the entire population. 58 % had an elevated NT-proBNP, while sST2 was abnormal in 40 %. Mean NT-proBNP was significantly higher in patients with severe PR (169 ± 150 vs145 ± 118, pg/ml, p < 0.001), while similar sST2 levels were observed in both groups (29 ± 14 vs30 ± 12, ng/ml, p > 0.05). NT-proBNP and sST2 levels were higher in patients with transannular patch when compared to other RVOT intervention (174 ± 145 vs 107 ± 100, pg/ml, p < 0.001); (31 ± 13 vs 29 ± 15, ng/ml, p < 0.05). Both biomarkers were significantly associated with exercise capacity, but NT-proBNP (r = −0.60, p < 0.001) was stronger. The optimal cut-off of 90 pg/ml for NT-proBNP had a sensitivity of 74 % and specificity of 63 % for detection of impaired exercise capacity. ConclusionsSerum levels of sST2 and NT-proBNP are elevated in patients with repaired TOF, with higher values observed in those with severe PR, but also in patients undergoing transannular patch repair. Incorporating both markers in these patients increased the ability to detect impairment in exercise capacity.

Soluble suppression of tumorigenicity 2 is a potential predictor of post-liver transplant renal outcomes.

Acute kidney injury is considered an independent prognostic factor for mortality in patients with liver cirrhosis. Non-treated acute kidney injury can progress to hepatorenal syndrome with a poor prognosis. As suppression of tumorigenicity 2 (ST2) is a member of the interleukin-1 receptor family that aggravates inflammation and fibrotic changes in multiple organs, we measured soluble ST2 (sST2) level in the serum and urine of liver-transplant recipients at the time of transplantation. The serum sST2 level significantly increased in liver-transplant recipients with suppressed kidney function compared with that in recipients with normal function. In recipients with severely decreased liver function (model for end-stage liver disease score ≥ 30), the serum sST2 level was higher than that in recipients with preserved liver function (model for end-stage liver disease score ≤ 20, P = 0.028). The serum sST2 level in recipients with hepatorenal syndrome was higher than that in liver-transplant recipients without hepatorenal syndrome (P = 0.003). The serum sST2 level in patients with hepatorenal syndrome was higher than that in recipients without a history of acute kidney injury (P = 0.004). Recipients with hepatorenal syndrome and recovered kidney function showed higher sST2 levels than those who did not recover (P = 0.034). Collectively, an increase in the serum sST2 level reflects a decrease in both kidney and liver functions. Thus, measuring sST2 level at the time of liver transplantation can help predict renal outcomes.

Exploring the significance of interleukin-33/ST2 axis in minimal change disease

Minimal change disease (MCD), a common cause of idiopathic nephrotic syndrome, has been postulated to exhibit an association with allergic conditions. Recent studies revealed the crucial role of interleukin (IL)-33 in type 2 innate immunity. We hypothesized that development of MCD involves an IL-33–related immune response. We examined 49 patients with biopsy-proven MCD, 6 healthy volunteers, and 29 patients in remission. In addition to clinical features, serum and urinary levels of IL-33 and soluble suppression of tumorigenicity 2 protein (sST2), a secreted form of the receptor of IL-33, were analyzed. Although IL-33 was barely detectable in either MCD or control samples, sST2 levels at diagnosis were elevated in MCD patients. Serum sST2 levels of MCD patients were correlated with serum total protein level (r = − 0.36, p = 0.010) and serum creatinine level (r = 0.34, p = 0.016). Furthermore, the elevated sST2 levels were observed to decrease following remission. Immunofluorescence revealed IL-33 expression in the podocytes among MCD patients, with a significant increase compared with controls. In vitro, mouse podocyte cells incubated with serum from a MCD patient at disease onset showed increased IL-33 secretion. These results suggest an IL-33–related immune response plays a role in MCD.

Clinical features, etiology, and survival in patients with restrictive cardiomyopathy: A single-center experience.

Numerous prognostic factors have been proposed for cardiac amyloidosis (CA). The knowledge about other subtypes of restrictive cardiomyopathy (RCM) is scant. This study aimed to elucidate the etiology and prognostic factors of RCM as well as assess cardiac biomarkers: high-sensitive troponin T (hs-TnT), growth differentiation factor-15 (GDF-15), N-terminal pro-B-type natriuretic peptide (NT-proBNP), and soluble suppression of tumorigenicity 2, as mortality predictors in RCM. We enrolled 36 RCM patients in our tertiary cardiac department. All patients were screened for CA. Genetic testing was performed in 17 patients without CA. Pathogenic or likely pathogenic gene variants were found in 86% of patients, including 5 novel variants. Twenty patients died, and 4 had a heart transplantation during the study. Median overall survival was 29 months (8-55). The univariate Cox models analysis indicated that systolic and diastolic blood pressure, GDF-15, hs-TnT, NT-proBNP, left ventricular stroke volume, the ratio of the transmitral early peak velocity (E) estimated by pulsed wave Doppler over the early mitral annulus velocity (e'), tricuspid annulus plane systolic excursion, early tricuspid valve annular systolic velocity, the presence of pulmonary hypertension, and pericardial effusion influenced survival (P <0.05). A worse prognosis was observed in patients with GDF-15 >1316 pg/ml, hs-TnT >42 ng/l, NT-proBNP >3383 pg/ml, and pericardial effusion >3.5 mm (Kaplan-Meier analysis, log-rank test, P <0.001). Genetic testing should be considered in every RCM patient where light-chain amyloidosis has been excluded. Survival remains poor regardless of etiology. Increased concentrations of GDF-15, hs-TNT, NT-proBNP, and pericardial effusion are associated with worse prognosis. Further studies are warranted.

Novel Biomarkers and Their Role in the Diagnosis and Prognosis of Acute Coronary Syndrome.

The burden of cardiovascular diseases and the critical role of acute coronary syndrome (ACS) in their progression underscore the need for effective diagnostic and prognostic tools. Biomarkers have emerged as crucial instruments for ACS diagnosis, risk stratification, and prognosis assessment. Among these, high-sensitivity troponin (hs-cTn) has revolutionized ACS diagnosis due to its superior sensitivity and negative predictive value. However, challenges regarding specificity, standardization, and interpretation persist. Beyond troponins, various biomarkers reflecting myocardial injury, neurohormonal activation, inflammation, thrombosis, and other pathways are being explored to refine ACS management. This review article comprehensively explores the landscape of clinically used biomarkers intricately involved in the pathophysiology, diagnosis, and prognosis of ACS (i.e., troponins, creatine kinase MB (CK-MB), B-type natriuretic peptides (BNP), copeptin, C-reactive protein (CRP), interleukin-6 (IL-6), d-dimers, fibrinogen), especially focusing on the prognostic role of natriuretic peptides and of inflammatory indices. Research data on novel biomarkers (i.e., endocan, galectin, soluble suppression of tumorigenicity (sST2), microRNAs (miRNAs), soluble oxidized low-density lipoprotein receptor-1 (sLOX-1), F2 isoprostanes, and growth differentiation factor 15 (GDF-15)) are further analyzed, aiming to shed light on the multiplicity of pathophysiologic mechanisms implicated in the evolution of ACS. By elucidating the complex interplay of these biomarkers in ACS pathophysiology, diagnosis, and outcomes, this review aims to enhance our understanding of the evolving trajectory and advancements in ACS management. However, further research is necessary to establish the clinical utility and integration of these biomarkers into routine practice to improve patient outcomes.

Importance of blood biomarker determination in the selection of patients with heart failure for cardioverterdefibrillator implantation

Aim. To conduct a comparative analysis of blood biomarker concentrations, to study their prognostic role in the occurrence of sustained ventricular tachyarrhythmia (VT) or VT episodes requiring electrotherapy in patients with heart failure (HF) and left ventricular ejection fraction (LVEF) ≤35% without prior syncope or sustained ventricular arrhythmias.Material and methods. This single-center prospective clinical study included 319 patients (men, 83%) aged 57 (51-63) years with LVEF of 29 (24-33)% receiving optimal therapy for HF, hospitalized for cardioverterdefibrillator implantation for the purpose of primary prevention of sudden cardiac death. Before the procedure, the concentration of blood biomarkers (blood electrolytes, C-reactive protein, creatinine, Soluble suppression of tumorigenicity 2 (sST2), N-terminal pro-brain natriuretic peptide (NT-proBNP), galectin-3) was determined. Based on blood creatinine concentration, glomerular filtration rate was calculated using the Chronic Kidney Disease Epidemiology Collaboration equation. Patients underwent a two-year prospective follow-up to record the end point of newly occurring clinically significant VT episodes detected by an implantable cardioverter-defibrillator.Results. The studied arrhythmic endpoint occurred in 84 (26,3%) patients. The multivariate analysis revealed three blood biomarkers, the concentration of which was associated with the first manifestation of VT. With sST-2 &gt;35 ng/ml, this risk increased by ~3 times (odds ratio (OR)=2,86; 95% confidence interval (CI): 1,23-6,64 (p=0,013)). Galectin-3 level &gt;12 ng/ml had a comparable prognostic value (OR=2,64; 95% CI: 1,06-6,53 (p=0,032)). In case of an increase in NT-proBNP &gt;2000 pg/ml, the risk of the same outcome was 2,2 times lower (OR=0,46; 95% CI: 0,22-0,95 (p=0,034)).Conclusion. Pre-implantation laboratory screening of NT-proBNP, sST-2 and galectin-3 concentrations can help in personalized assessment of arrhythmic risk in patients with HF and LVEF ≤35% referred for interventional primary prevention of sudden cardiac death.

Significance of sTREM-1 and sST2 combined diagnosis for sepsis detection and prognosis prediction.

The diagnosis of sepsis still lacks a practical and reliable gold standard. The purpose of this study was to confirm the effect of soluble triggering receptor expressed on myeloid cells-1 (sTREM-1) combined with soluble suppression of tumorigenicity 2 (sST2) in the diagnosis of sepsis through the correlation between sTREM-1, sST2, and sequential organ failure assessment (SOFA) scores. Baseline data of 91 patients with sepsis in the intensive care unit were collected, sTREM-1 and sST2 were detected, and the correlation between markers and SOFA score was analyzed. Besides, the prognostic value of baseline and postadmission indicators for sepsis was analyzed with death as the outcome. The results showed that the expressions of sST2 and sTREM-1 in death group and survival group were higher than those in the survival group (p < 0.05). Correlation analysis showed that sST2, sTREM-1, and the joint diagnosis model had a high correlation with SOFA score (p < 0.05), but poor correlation with Acute Physiology and Chronic Health Evaluation Ⅱ score (p > 0.05). Among them, joint diagnosis model has the highest correlation. Receiver operating characteristic curve analysis showed that combined diagnosis had higher area under curve values. sTREM-1/sST2 can be better used in the diagnosis of sepsis than the single biomarker detection, and the combination of the above two biomarkers has potential application value in the detection and prognosis prediction of sepsis.

Circulating Gal-3 and sST2 are associated with acute exercise-induced sustained endothelial activation: Possible relevance for fibrosis development?

Long-term, intense endurance exercise training can occasionally induce endothelial micro-damage and cardiac fibrosis. The underlying mechanisms are incompletely understood. Twenty healthy, well-trained male participants (10runners and 10cyclists) performed a strenuous high-intensity interval training (HIIT) session matched by age, height, weight and maximal oxygen consumption. We assessed the acute exercise response of novel cardiac biomarkers of fibrosis [e.g., galectin-3 (Gal-3) and soluble suppression of tumorigenicity 2 (sST2)] per exercise modality and their relationship with haemodynamic contributors, such as preload, afterload and cardiac contractility index (CTi), in addition to endothelial damage by sustained activation and shedding of endothelial cells (ECs). Serum Gal-3 and sST2 concentrations were investigated by enzyme-linked immunosorbent assays; haemodynamics were analysed via impedance plethysmography and circulating ECs by flow cytometry. The Gal-3 and sST2 concentrations and ECs were elevated after exercise (P<0.001), without interaction between exercise modalities. Circulating Gal-3 and sST2 concentrations both showed a positive relationship with ECs (rrm =0.68, P=0.001 and rrm =0.57, P=0.010, respectively, both n=18). The EC association with Gal-3 was significant only in cyclists, but equally strong for both modalities. Gal-3 was also related to exercise-induced CTi (rrm =0.57, P=0.011, n=18). Cardiac wall stress is increased after an acute HIIT session but does not differ between exercise modalities. Exercise-released Gal-3 from cardiac macrophages could very probably drive systemic endothelial damage, based on an enhanced CTi. The importance of acute exercise-induced vascular resistances and cardiac contractility for the release of fibrotic biomarkers and any long-term pathological endothelial adaptation should be investigated further, also relative to the exercise modality. NEW FINDINGS: What is the central question of this study? Circulating biomarkers of cardiac wall stress and fibrosis are influenced by physical exercise. The underlying mechanisms per exercise modality are still unclear. What is the main finding and its importance? We show that galectin-3 (Gal-3) and soluble suppression of tumorigenicity 2 (sST2) are increased after acute exercise but do not differ between running and cycling. One haemodynamic contributor to the secretion of Gal-3 is an enhanced cardiac contractility. Acute exercise-released Gal-3 and sST2 are linked to sustained endothelial activation and cell shedding. This could be relevant in the context of fibrosis development and could identify athletes at risk for pathological endothelial adaptations.