Changes In Galectin-3 Research Articles

Role of Galectin-3 in intervertebral disc degeneration: an experimental study

BackgroundThis study investigated the role of Galectin-3 in the degeneration of intervertebral disc cartilage.MethodsThe patients who underwent lumbar spine surgery due to degenerative disc disease were recruited and divided into Modic I, Modic II, and Modic III; groups. HE staining was used to detect the pathological changes in endplates. The changes of Galectin-3, MMP3, Aggrecan, CCL3, and Col II were detected by immunohistochemistry, RT-PCR, and Western blot. MTT and flow cytometry were used to detect cartilage endplate cell proliferation, cell cycle, and apoptosis.ResultsWith the progression of degeneration (from Modic I to III), the chondrocytes and density of the cartilage endplate of the intervertebral disc decreased, and the collagen arrangement of the cartilage endplate of the intervertebral disc was broken and calcified. Meanwhile, the expressions of Aggrecan, Col II, Galectin-3, Aggrecan, and CCL3 gradually decreased. After treatment with Galectin-3 inhibitor GB1107, the proliferation of rat cartilage end plate cells was significantly reduced (P < 0.05). GB1107 (25 µmol/L) also significantly promoted the apoptosis of cartilage endplate cells (P < 0.05). Moreover, the percentage of cartilage endplate cells in the G1 phase was significantly higher, while that in the G2 and S phases was significantly lower (P < 0.05). Additionally, the mRNA and protein expression levels of MMP3, CCL3, and Aggrecan in rat cartilage end plate cells were lower than those in the control group.ConclusionsGalectin-3 decreases with the progression of the cartilage endplate degeneration of the intervertebral disc. Galectin-3 may affect intervertebral disc degeneration by regulating the degradation of the extracellular matrix.

Biomarkers and Strain Echocardiography for the Detection of Subclinical Cardiotoxicity in Breast Cancer Patients Receiving Anthracyclines.

The optimal surveillance and management strategies for breast cancer patients receiving anthracycline therapy are limited by our incomplete understanding of the role of biomarkers heralding the onset of cardiotoxicity. The purpose of this study was to determine whether there is a temporal correlation between cardiac biomarkers and subclinical left ventricular dysfunction in breast cancer patients receiving anthracycline chemotherapy. Thirty-one females between 46 and 55 years old with breast cancer treated with anthracycline chemotherapy were prospectively enrolled. Cardiac biomarkers were correlated with echocardiography with speckle tracking at baseline, post-anthracycline therapy, and 6 months post-anthracycline chemotherapy. Subclinical cardiotoxicity was defined as ≥ 10% reduction in global longitudinal strain (GLS). There was a relative reduction in left ventricular ejection fraction (LVEF) ≥ 10% in 5/30 (17%) and 7/27 (26%) patients post-anthracycline therapy and 6 months post-anthracycline therapy, respectively. Subclinical cardiotoxicity was noted in 8/30 (27%) and 10/26 (38%) patients post-anthracycline and 6 months post-anthracycline therapy, respectively. Baseline N-terminal pro B-type natriuretic peptide (NT-proBNP) was the strongest predictor of LVEF (ρ = -0.45; p = 0.019), with post-therapy NT-proBNP values illustrating similar predictive value (ρ = -0.40; p = 0.038). Interim changes in suppression of tumorigenicity 2 (ST2) and galectin-3 correlated with a 6-month change in LVEF (ρ = -0.48; p = 0.012 and ρ = -0.45; p = 0.018, for ST2 and galectin-3, respectively). Changes in galectin-3 from baseline to mid-therapy paralleled changes in GLS. NT-proBNP, ST2, and galectin-3 correlate with reduced LVEF among breast cancer patients receiving anthracycline therapy. Additional trials focusing on a cardiac biomarker approach may provide guidance in the early diagnosis and management of anthracycline-induced cardiotoxicity.

Intermittent fasting and changes in Galectin-3: A secondary analysis of a randomized controlled trial of disease-free subjects

Background and aimsIntermittent fasting reduces risk of interrelated cardiometabolic diseases, including type 2 diabetes and heart failure (HF). Previously, we reported that intermittent fasting reduced homeostasis model assessment of insulin resistance (HOMA-IR) and Metabolic Syndrome Score (MSS) in the WONDERFUL Trial. Galectin-3 may act to reduce insulin resistance. This post hoc evaluation assessed whether intermittent fasting increased galectin-3. Methods and resultsThe WONDERFUL Trial enrolled adults ages 21–70 years with ≥1 metabolic syndrome features or type 2 diabetes who were not taking anti-diabetic medication, were free of statins, and had elevated LDL-C. Subjects were randomized to water-only 24-h intermittent fasting conducted twice-per-week for 4 weeks and once-per-week for 22 weeks or to a parallel control arm with ad libitum energy intake. The study evaluated 26-week change scores of galectin-3 and other biomarkers. Overall, n = 67 subjects (intermittent fasting: n = 36; control: n = 31) completed the trial and had galectin-3 results. At 26-weeks, the galectin-3 change score was increased by intermittent fasting (median: 0.793 ng/mL, IQR: −0.538, 2.245) versus control (median: −0.332 ng/mL, IQR: −0.992, 0.776; p = 0.021). Galectin-3 changes correlated inversely with 26-week change scores of HOMA-IR (r = −0.288, p = 0.018) and MSS (r = −0.238, p = 0.052). Other HF biomarkers were unchanged by fasting. ConclusionA 24-h water-only intermittent fasting regimen increased galectin-3. The fasting-triggered galectin-3 elevation was inversely correlated with declines in HOMA-IR and MSS. This may be an evolutionary adaptive survival response that protects human health by modifying disease risks, including by reducing inflammation and insulin resistance. Trial registrationClinicaltrials.gov, NCT02770313 (registered on May 12, 2016; first subject enrolled: November 30, 2016; final subject's 26-week study visit: February 19, 2020).

Abstract 10312: Intermittent Fasting and Increased Galectin-3 Reveal a Potential Protective Mechanism Against Risk of Heart Failure and Type 2 Diabetes

Introduction: Intermittent fasting decreases cardiometabolic risk factors, heart failure (HF) risk, and type 2 diabetes risk. Sodium-glucose transport 2 (SGLT-2) inhibitors reduce diabetes and HF risk and a study of canagliflozin reported that it raised galectin-3 levels (Januzzi 2017). Previously in the WONDERFUL trial (NCT02770313), intermittent fasting caused declines in the Metabolic Syndrome Score (MSS) and homeostatic model assessment of insulin resistance (HOMA-IR). This study evaluated intermittent fasting’s effects on galectin-3 in a post hoc analysis of the WONDERFUL Trial. Methods: People aged 21-70 years were enrolled who had ≥1 metabolic syndrome feature or type 2 diabetes, were free of anti-diabetic and statin medications, and had elevated LDL-C. Subjects had 26-week galectin-3 data (N=67; n=36 intermittent fasting, n=31 controls). Subjects were randomized to a 24-hour water-only fasting intervention (fasting twice per week for 4 weeks, then once each week for 22 weeks) or a parallel control arm ( ad libitum eating). This study evaluated the 26-week galectin-3 change score and other changes in HF biomarkers. Results: At 26 weeks, the galectin-3 change score was increased in intermittent fasting (0.575±2.63 ng/mL) vs control (-0.624±2.79 ng/mL; p=0.021). Changes in galectin-3 were inversely correlated with HOMA-IR change score (r= -0.288, p=0.018) and MSS change score (r= -0.238, p=0.052). Changes in galectin-3 at 4 weeks (intermittent fasting: 0.345±2.68 ng/mL; control: -0.465±3.18 ng/mL; p=0.27) and 13 weeks (fasting: 0.917±4.96; control: -0.097±2.83 ng/mL; 0.15) were not significantly different. B-type natriuretic peptide went down in intermittent fasting (-0.328±12.29 pg/mL) but this was not significant compared to controls (15.50±75.34 pg/mL, p=0.23). Other HF biomarkers were unchanged. Conclusions: Water-only 24-hour intermittent fasting increased galectin-3. This rise in galectin-3 was correlated with declining HOMA-IR and MSS and may be similar to reported effects of SGLT-2 inhibitors. Increased galectin-3 may be an adaptive response that could prevent chronic disease by decreasing inflammation, ameliorating insulin resistance, or modifying related mechanisms.

Correlation Study of Galectin-3 in Patients with an Ascending Aortic Aneurysm and Ventricular Remodeling Before and After Surgical Correction.

ObjectiveThe present study aims to observe the changes in galectin-3 (Gal-3) expression levels in patients with an ascending aortic aneurysm and ventricular remodeling and analyze Gal-3’s correlation with ventricular remodeling.MethodsA total of 102 patients with an ascending aortic aneurysm were included as the research subjects. Gal-3 expression levels in the peripheral blood of the patients were detected by an enzyme-linked immunosorbent assay before the operation and then three and six months after. The left ventricular ejection fraction (LVEF), left ventricular end-diastolic diameter (LVEDD), interventricular septal thickness, and left ventricular posterior wall thickness were recorded, and the left ventricular mass index (LVMI) was calculated. Changes in Gal-3 expression levels, LVMI, LVEF, and LVEDD were observed before and after surgery, and these changes were then analyzed.ResultsThere were significant differences in Gal-3 expression levels, LVMI, and LVEDD before surgery and three months after (P < 0.001) but no significant difference in LVEF (P = 0.887). There were significant differences in Gal-3 expression levels, LVMI, LVEDD, and LVEF (P < 0.05) three and six months after surgery. Before surgery and three and six months after surgery, Gal-3 was positively correlated with LVMI and LVEDD (R = 0.697, R = 0.571, and R = 0.454, respectively), and a receiver operating characteristic curve found that Gal-3 was able to predict ventricular remodeling, with an area under the curve value of 0.721.ConclusionGal-3 expression levels are correlated with ascending aortic aneurysms combined with ventricular remodeling, which provides a reference value for predicting ventricular remodeling.

Correlation between Galectin-3 and Early Herpes Zoster Neuralgia and Postherpetic Neuralgia: A Retrospective Clinical Observation.

This study aims to explore the value of serum galectin-3 in patients with herpes zoster neuralgia (HZN) and postherpetic neuralgia (PHN) and other factors influencing HZN and PHN occurrence. Samples from forty patients with herpes zoster neuralgia (HZN) (Group H), 40 patients with nonherpes zoster neuralgia (Group N), and 20 cases of health check-up were collected. Patients were divided into PHN group (Group A) and non-PHN group (Group B) according to the occurrence of PHN in Group H. Galectin-3, T-lymphocyte subsets, and IL-6 were recorded in all patients. The changes of galectin-3 in patients with early HZN and PHN were analyzed by single-factor analysis and multifactor analysis. The age (P=0.012) and NRS scores (P < 0.001) of PHN patients were significantly higher than those of non-PHN patients and other neuralgia patients. The ratio of CD3+ (F = 80.336, P < 0.001), CD4+ (F = 12.459, P < 0.001) lymphocyte subsets, and CD4+/CD8+ (F = 15.311, P < 0.001) decreased significantly in PHN patients. The level of blood IL-6 (F = 139.446, P < 0.001) in PHN patients was significantly increased. Serum galectin-3 was significantly higher in HZN patients than in PHN patients (P < 0.05); IL-6 (OR = 10.002, 95% CI: 3.313–30.196, P < 0.001) and galectin-3 (OR = 3.719, 95% CI: 1.261–10.966, P=0.017) were the risk factors for HZN; galectin-3 (OR = 17.646, 95% CI: 2.795–111.428, P=0.002) was also the risk factor for PHN. ROC curve analysis also showed that serum galectin-3 was a better predictor of poor prognosis (AUC = 0.934, P < 0.001). Therefore, as an independent risk factor of HZN and PHN, serum galectin-3 may be used as a new biochemical marker in clinical practice.

Abstract #216 Absence of Changes in Galectin-3 with Insulin Sensitization and Antiinflammation

Abstract #216 Absence of Changes in Galectin-3 with Insulin Sensitization and Antiinflammation

Serum Galectin-3 Levels in Patients with Hepatocellular Carcinoma, Liver Cirrhosis and Chronic Viral Hepatitis

Background: hepatocellular carcinoma (HCC) represents a global health problem. It is the fifth most common solid tumor and the third cause of cancer-related mortality per year.In Egypt, it represents 75% of malignant liver tumors. Early detection and diagnosis of these cases are required for successful treatments and improved outcomes. Aim of the Work: this study aimed to detect serum galactin-3 levels in patients with HCC, liver cirrhosis and chronic viral hepatitis (HBV, or HCV) patients. Patients and Methods: this prospective study was conducted on a total of 60 patients, 20 of them with chronic viral hepatitis B or C, 20 with cirrhosis secondary to chronic viral hepatitis and 20 with HCC secondary to chronic viral hepatitis. It was carried out at the Clinical Pathology Department, Tanta University Hospital. Results: the mean galectin‑3 levels were 15.5 ng/mL (±5.5) in HCC patients, 20.46 ng/mL (±7.56) in cirrhotic patients and 7.003 ng/mL (±4.24) in chronic viral hepatitis group. There were statistical differences between HCC and cirrhotic patients (P< 0.03), but they were lower in chronic hepatitis group statistically compared to cirrhosis and HCC (P< 0.001). Conclusion: serum galectin‑3 levels in patients with chronic HBV or HCV may guide us about progression to cirrhosis or HCC and prognosis of the disease. In these patients, if galectin‑3 levels were found to be high, serum alpha‑feto protein level and ultrasonographic examination could be repeated at more frequent intervals. This may also guide us in terms of the treatment plan. Recommendations: it was recommended to measure changes of galectin-3 in hepatitis carries. Measurement of galectin-3 in a large scale of patients to explore its prognostic value.

Galectin-3 in patients with coronary heart disease and atrial fibrillation

ObjectiveTo observe the change of the inflammatory factor Galectin-3 in patients with coronary heart disease, and the correlation between Galectin-3 and the severity of the disease. To observe changes of Galectin-3 in patients with atrial fibrillation (AF) before and after radiofrequency ablation, and the changes of Galectin-3 before and after an interim treatment with a high dose of atorvastatin on patients with acute myocardial infarction(AMI). MethodsPatients with coronary heart disease and atrial fibrillation having normal heart function were selected, among them, the patients with AMI were given a short term treatment of 80mg atorvastatin before PCI, and patients with atrial fibrillation underwent radiofrequency catheter ablation. ELISA technique was equipped to observe the Galectin-3 changes in patients with coronary heart disease and that of patients with AF before and after radiofrequency ablation. ResultsGalectin-3 level of the AMI group was higher than that of the unstable angina pectoris (UAP) group, and its levels were higher than that of the stable angina pectoris (SAP) group, the differences were statistically significant among both groups (P<0.05); Galectin-3 level of multivessel coronary disease group was higher than that of single vessel group, in which a statistically significant difference was noted (P<0.05); There was no statistically significant difference associated in the drop of Galectin-3 levels in patients with AMI after PCI (P>0.05); Galectin-3 of patients with AF decreased after RFCA, but no statistical significance noted (P>0.05); Galectin-3 was negatively correlated with the LVEF value(r=−0.405, P<0.05). ConclusionGalectin-3 belongs to a class of inflammatory mediators that is associated with the degree of myocardial inflammation and fibrosis. It is related to the severity of myocardial ischemia and is negatively correlated with the cardiac ejection fraction.

Determinants of temporal changes in galectin-3 level in the general population: Data of PREVEND

BackgroundHigh baseline galectin-3 levels are associated with increased risk for adverse cardiovascular outcomes in the general population, but determinants of changes in galectin-3 levels over time have not been established. Therefore, we aimed to identify determinants of (temporal) change in galectin-3 levels. MethodsGalectin-3 plasma levels were measured in a large community based cohort (PREVEND study) at 3 different time points: at baseline, after ~4 and ~9years. The association of baseline clinical and biochemical factors and (temporal) changes in galectin-3 level was assessed using multivariable mixed-effects regression modeling. ResultsIn 4355 subjects, galectin-3 plasma levels were available at all time points (mean age: 48±12years; 50% female). Median galectin-3 level at baseline was 10.7 [8.9–12.7] ng/mL which gradually increased to 11.5 [9.4–14.3] ng/mL after ~9years. Using mixed-effects regression modeling, we first validated as independent determinants of baseline circulating galectin-3: eGFR (chi square (χ2):210.27, p<0.0001), gender (χ2:43.85; p<0.0001), BMI (χ2:19.68, p=0.0001), NT-proBNP (χ2:18.76, p=0.0001) and serum (total) cholesterol (χ2:8.63, p=0.01). Furthermore, we identified urinary albumin excretion (χ2:34.03, p-value: <0.0001) and systolic blood pressure (χ2:16.81, p=0.002) as independent determinants of temporal changes of galectin-3. ConclusionsIn the general population, urinary albumin excretion >30mg/24h and systolic blood pressure >170mmHg were identified as significant determinants of dynamic increases in galectin-3 levels over time. These results implicate that treatment of high blood pressure might be effective to prevent increasing galectin-3 levels and its associated conditions.

DIAGNOSTIC SIGNIFICANCE OF NOVEL MARKERS FOR ASSESSMENT OF MYOCARDIUM CONDITION IN OBSTRUCTIVE DIFFUSE-GENERALIZED FORM OF HYPERTROPHIC CARDIOMYOPATHY

Aim . To evaluate informativity and relation of changes of galectin-3 (G3) and natriuretic brain peptide (BNP) in diagnostics of myocardium dysfunctions during analysis of surgical intervention in HCMP patients. Material and methods . An analysis is presented, of 30 patients with diffusegeneralized type of hypertrophic cardiomyopathy (HCMP) (16 females and 14 males, mean age 53,7±2,8 y. o.), who during the time from 2009 to may 2016 in V. B. Petrovskiy Russian National Research Centre of Surgery, underwent the operation of extended myectomy. Before and after operation all patients underwent laboratory tests with measurement of the levels of BNP and G3 in serum, echocardiography, MRI/MSCT of the heart. Operations were done on-pump and pharmaco-cold cardioplegy. Results. In transthoracal echocardiography there was significant decrease revealed, of interventricular septum thickness and gradient of ascending LV tractus, and nonsignificant enlargement of LV cavity during systole. In analysis of i. v. contrast MRI/MSCT of the heart in 26 patients there was non-significant increase of LV cavity during systole and decrease of LV mass in diastole. In analysis of serum BNP level as an important marker of clinical course and treatment efficacy, there was significant decrease of the values comparing to baseline in pre-operation period. Conclusion. The extended myectomy surgery with parietal resection of papillary muscles makes it to reach good effect on an interventricular pressure gradient elimination in the space of whole ascending tractus of the left ventricle. Comparing to BNP that make it possible to evaluate the effectiveness of treatment, G3 is not so effective in diagnostics and there is yet no convincing evidence to confirm the value of G3 concentration in blood as an instrument that can be applied in monitoring of surgery effect.

Galectin-3 contributes to cisplatin-induced myeloid derived suppressor cells (MDSCs) recruitment in Lewis lung cancer-bearing mice

Recently the recruitment/migration of myeloid derived suppressor cells (MDSCs) to tumor microenvironment after chemotherapy has attracted much attention. To determine the detailed mechanism for the responses of MDSCs to these chemotherapies, we investigated the changes of galectin-3 and MDSCs in response to cisplatin(0.4 mg/kg, 4 mg/kg) treatment both in vivo and ex vivo. In the process of cisplatin, we assessed levels of galectin-3 and MDSCs in the Lewis lung cancer (LLC) bearing mice using immunohistochemistry, enzyme-linked immunosorbent assay (ELISA), immunofluorence and flow cytometry (FCM). The expression and changes of galectin-3 in the LLC cell line were detected by western blot, immunofluorence and ELISA. The ligand for galectin-3 on MDSCs and the chemotaxis of galectin-3 to MDSCs were confirmed using FCM and transwell. Parallel increased level of galectin-3 with the number of MDSCs in vivo was detected after cisplatin treatment. LLC cells expressed galectin-3 and cisplatin increased galectin-3 level in the culture medium. Furthermore, MDSCs were detected to express CD98, the ligand of galectin-3, and could be recruited by galectin-3. Our results suggested that the elevated expression of gelectin-3 in LLC tumor cells may contribute to the migration of MDSCs to the tumor microenvironment in response to cisplatin.

Galectin-3: its role in asthma and potential as an anti-inflammatory target

Galectins constitute an evolutionary conserved family that bind to β-galactosides. Increasing evidence shows that galectins are involved in many fundamental biological processes such as cellular communication, inflammation, differentiation and apoptosis. Changes in galectin-3 (Gal-3) expression are commonly seen in cancer and pre-cancerous conditions, and Gal-3 may be involved in the regulation of diverse cancer cell activities that contribute to tumourigenesis, cancer progression and metastasis. In addition, Gal-3 is a pro-inflammatory regulator in rheumatoid arthritis. Gal-3 has been shown to be involved in many aspects in allergic inflammation, such as eosinophil recruitment, airway remodeling, development of a Th2 phenotype as well as increased expression of inflammatory mediators. In an in vivo model it was shown that bronchoalveolar lavage (BAL) fluid from ovalbumin-challenged mice contained significantly higher levels of Gal-3 compared to control mice. The molecular mechanisms of Gal-3 in human asthma have not been fully elucidated. This review will focus on what is known about the Gal-3 and its role in the pathophysiological mechanisms of asthma to evaluate the potential of Gal-3 as a biomarker and therapeutic target of asthma.

Baseline and serial measurements of galectin‐3 in patients with heart failure: relationship to prognosis and effect of treatment with valsartan in the Val‐HeFT

This study was conducted to determine whether galectin-3, a β-galactoside-binding lectin, plays a role in the pathogenesis of heart failure (HF). Galectin-3 was measured at baseline (n = 1650), after 4 months (n = 1346), and after 12 months (n = 1097) in the Valsartan Heart Failure Trial (Val-HeFT). Galectin-3 levels at baseline ranged from 4.8 to 53 ng/mL. Higher levels were associated with features of worse HF. In a fully adjusted Cox regression model comprising 23 other prognostic variables, baseline galectin-3 was not associated with the risks of all-cause mortality, the composite of the first morbid event, or hospitalization for HF. However, when changes in galectin-3 over time were examined, the increases in galectin-3 between baseline and 4 months were independently and significantly associated with the risks of subsequent all-cause mortality, first morbid event, and hospitalizations for HF, even after adjusting for all baseline and concurrent changes in all variables including estimated glomerular filtration rate (eGFR) and NT-proBNP. The strongest correlate of galectin-3 levels was eGFR, which accounted for 20% of the variability in galectin-3 levels at baseline. There was a significant interaction (P = 0.03) between baseline galectin-3 and the effect of valsartan on hospitalizations for HF. Valsartan caused a significant 44% reduction in hospitalizations for HF in patients with galectin-3 levels below the median level of 16.2 ng/mL, but not in patients with levels above the median. Galectin-3 levels are elevated in a substantial proportion of patients with HF, particularly those with more severe HF and renal dysfunction. Galectin-3 increased over time in this cohort, and the increase was independently associated with worse outcomes. Valsartan use was associated with a reduction in hospitalizations for HF in patients with low galectin-3, but not in those with higher levels of galectin-3.

Changes in Galectin-3 Levels over Time Predict Mortality and Morbidity in Chronic HF

Background: Elevated circulating levels of galectin-3, a protein implicated in myocardial fibrosis and remodeling, are associated with significantly increased risk of morbidity and mortality among chronic heart failure (HF) subjects. The clinical utility of serial measurements of galectin-3, however, has not been reported. Methods: Galectin-3 was measured at baseline and at 3 months in a study comprising 1,329 subjects of the Controlled Rosuvastatin Multinational Trial in Heart Failure (CORONA), and at baseline and 6 months in 324 subjects of the Coordinating Study Evaluating Outcomes of Advising and Counseling in Heart Failure (COACH). An assay recently cleared by the U.S. Food and Drug Administration was used to measure galectin-3, and the indicated threshold value of 17.8 ng/mL was adopted to categorize subjects into 4 categories: subjects whose galectin-3 values remained either below or above 17.8 ng/mL, and subjects whose galectin-3 levels either increased or decreased between baseline and the second sampling time point. Results: Categorical changes in galectin-3 were observed in 17.3% of subjects from CORONA over 3 months, and 23.5% of subjects from COACH over 6 months. For the composite endpoint of total mortality and HF hospitalization, the outcome of subjects with a low baseline galectin-3 level that increased over time was significantly worse than that of subjects that maintained a low level (Cox hazard ratio (HR) in CORONA, 1.60 (95% CI: 1.152.22), p50.005; HR in COACH, 2.46 (95% CI: 1.05-5.73, p50.037)). Similarly, subjects with a high baseline level that decreased over time exhibited significantly fewer endpoints than subjects that remained high over time (HR in CORONA, 0.68 (95% CI: 0.49-0.94), p50.020; HR in COACH, 0.48 (95% CI: 0.27-0.87), p50.015). Analyses of multiple secondary endpoints yielded comparable results. Conclusions: In two large cohorts of chronic HF subjects, serial measurements of galectin-3 concentration are shown to provide important and significant prognostic value for morbidity and mortality risk assessment. 295