Faculty Opinions recommendation of Head-to-head comparison of 2 myocardial fibrosis biomarkers for long-term heart failure risk stratification: ST2 versus galectin-3.

Author(s):  
Marrick Kukin ◽  
Saurav Chatterjee ◽  
Manpreet Singh Sabharwal
2014 ◽  
Vol 63 (2) ◽  
pp. 158-166 ◽  
Author(s):  
Antoni Bayes-Genis ◽  
Marta de Antonio ◽  
Joan Vila ◽  
Judith Peñafiel ◽  
Amparo Galán ◽  
...  

2015 ◽  
Vol 65 (10) ◽  
pp. A773
Author(s):  
Giulia Magnani ◽  
Michelle O’Donoghue ◽  
Eugene Braunwald ◽  
Dylan Steen ◽  
Petr Jarolim ◽  
...  

Author(s):  
Janka Franeková ◽  
Zdeněk Kubíček ◽  
Lenka Hošková ◽  
Markéta Kotrbatá ◽  
Peter Sečník ◽  
...  

AbstractGalectin-3 is an emerging biomarker of heart failure and of myocardial fibrosis risk. Monitoring of galectin-3 is essential during treatment with galectin-3 inhibitors. The aim of our study was to assess long-term biological variability in a specific group of unhealthy subjects.The biological variability of galectin-3 was measured in a group of 44 patients after heart transplantation (HTx). Six samples were taken from each patient during a 12-month period. Galectin-3 was measured with an Abbott Architect automated immunoassay.Intraindividual (CVThe concentrations of galectin-3 in patients followed 12 months after HTx fluctuated around the homeostatic point, with CV


2010 ◽  
Vol 6 (2) ◽  
pp. 33 ◽  
Author(s):  
Christopher R deFilippi ◽  
G Michael Felker ◽  
◽  

For many with heart failure, including the elderly and those with a preserved ejection fraction, both risk stratification and treatment are challenging. For these large populations and others there is increasing recognition of the role of cardiac fibrosis in the pathophysiology of heart failure. Galectin-3 is a novel biomarker of fibrosis and cardiac remodelling that represents an intriguing link between inflammation and fibrosis. In this article we review the biology of galectin-3, recent clinical research and its application in the management of heart failure patients.


2016 ◽  
Vol 62 (2) ◽  
pp. 360-366 ◽  
Author(s):  
Emily I Schindler ◽  
Jeffrey J Szymanski ◽  
Karl G Hock ◽  
Edward M Geltman ◽  
Mitchell G Scott

Abstract BACKGROUND Galectin-3 (Gal-3) has been suggested as a prognostic biomarker in heart failure (HF) patients that may better reflect disease progression than traditional markers, including B-type natriuretic peptide (BNP) and cardiac troponins. To fully establish the utility of any biomarker in HF, its biologic variability must be characterized. METHODS To assess biologic variability, 59 patients were prospectively recruited, including 23 male and 16 female patients with stable HF and 10 male and 10 female healthy individuals. Gal-3, BNP, and high-sensitivity cardiac troponin I (hs-cTnI) were assayed at 5 time points within a 3-week period to assess short-term biologic variability. Long-term (3-month) biologic variability was assessed with samples collected at enrollment and after 4, 8, and 12 weeks. RESULTS Among healthy individuals, mean short-term biologic variability, expressed as intraindividual CV (CVI), was 4.5% for Gal-3, 29.0% for BNP, and 14.5% for hs-cTnI; long-term biologic variability was 5.5% for Gal-3, 34.7% for BNP, and 14.7% for hs-cTnI. In stable HF patients, mean short-term biologic variability was 7.1% for Gal-3, 22.5% for BNP, and 8.5% for hs-cTnI, and mean long-term biologic variability was 7.7% for Gal-3, 27.6% for BNP, and 9.6% for hs-cTnI. CONCLUSIONS The finding that Gal-3 has minimal intraindividual biological variability adds to its potential as a useful biomarker in HF patients.


Author(s):  
Vincenzo Castiglione ◽  
Alberto Aimo ◽  
Giuseppe Vergaro ◽  
Luigi Saccaro ◽  
Claudio Passino ◽  
...  

AbstractHeart failure (HF) is a significant cause of morbidity and mortality worldwide. Circulating biomarkers reflecting pathophysiological pathways involved in HF development and progression may assist clinicians in early diagnosis and management of HF patients. Natriuretic peptides (NPs) are cardioprotective hormones released by cardiomyocytes in response to pressure or volume overload. The roles of B-type NP (BNP) and N-terminal pro-B-type NP (NT-proBNP) for diagnosis and risk stratification in HF have been extensively demonstrated, and these biomarkers are emerging tools for population screening and as guides to the start of treatment in subclinical HF. On the contrary, conflicting evidence exists on the role of NPs as a guide to HF therapy. Among the other biomarkers, high-sensitivity troponins and soluble suppression of tumorigenesis-2 are the most promising biomarkers for risk stratification, with independent value to NPs. Other biomarkers evaluated as predictors of adverse outcome are galectin-3, growth differentiation factor 15, mid-regional pro-adrenomedullin, and makers of renal dysfunction. Multi-marker scores and genomic, transcriptomic, proteomic, and metabolomic analyses could further refine HF management.


2014 ◽  
Vol 103 (suppl 1) ◽  
pp. S89.2-S89
Author(s):  
B Lopez Salazar ◽  
A Gonzalez Miqueo ◽  
R Querejeta Iraola ◽  
M Larman Tellechea ◽  
J Diez Martinez

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Nisha Plavelil ◽  
Mark C Haigney ◽  
Robert E Goldstein ◽  
Michael Klein ◽  
Matie Shou ◽  
...  

Introduction: Although frequently used in heart failure (HF), long-term furosemide exacerbates HF in a swine model. This paradoxical phenomenon may reflect furosemide-induced alterations in signaling proteins of the extracellular matrix (ECM) to increase fibrosis. Examination of the ECM may clarify how treatments like furosemide enhance the progression of HF. Hypothesis: The administration of furosemide increased inflammation and fibrosis of the heart, leading to accelerated HF deterioration in a swine model. Methods: After Institutional Animal Care and Use Committee (IACUC) approval, Yorkshire swine (N=10, 5 = furosemide, 5 = saline) were paced 3 to 5 weeks at 200 beats per minute to induce HF (left ventricular fractional shortening <16% on echocardiogram). Animals were treated with furosemide (1 mg/kg intramuscularly) or saline. Western Blot and histology with Masson’s trichrome stain were performed on transmural LV myocardium to quantify critical determinants of fibrosis. ANOVA with Tukey HSD correction and descriptive statistics were performed using SPSS with significance by α of 0.05; mean ± SEM. Results: The overall increase in ECM fibrosis in HF was clearly demonstrated on Masson’s trichrome histology associated with significant, uniform increase in signaling pathways leading to fibrosis associated with furosemide use. SMAD 2-HF Furosemide to Control (p<.05): HF Furosemide 0.266 ±.05, HF Saline 0.183±.02, Control 0.163±.01 ERK-all (p<.05): HF Furosemide 0.312±.02, HF Saline 0.209±.01,Control 0.149±.01 GDF-15-HF Furosemide to Control (p<.05): HF Furosemide 0.095 ±.00, HF Saline 0.073±.01, Control 0.062±.01 MMP-14-all (p<.05): HF Furosemide 0.451±.02, HF Saline 0.374±.03,Control 0.231±.02 TIMP-1-all (p<.05): HF Furosemide 0.184±.01, HF Saline 0.0135±.03,Control 0.033±.01 PAI-1-all (p<.05): HF Furosemide 0.105±.01, HF Saline 0.046±.01,Control 0.043±.00 Conclusions: Histologic and biochemical analysis showed worsening HF in furosemide-treated paced swine was associated with consistent increases in fibrosis and indices of adverse ECM remodeling. The diuretic intended to reduce water retention during HF appeared to enhance myocardial fibrosis, paradoxically accelerating pathological processes responsible for HF.


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